Miracle-dz/UniFAR-FTUs huggingface dataset:
Short-Term and Long-Term-Effects of Phorbol 12-Myristate 13-Acetate and Different Inhibitors on the Ability of Bone Marrow Cells to Form Colonies In Vitro

The process of signal transduction responsible for the phorbol 12-myristate 13-acetate mediated increase in the colony-forming potential of murine (CBA) bone marrow cells was studied using known modulators of the mitogenic signal. Pretreatment of cells for 60 minutes with staurosporine (1 mumol/l), an inhibitor of protein kinase C, completely prevented colony formation in the control group of cells and significantly reduced the number of colonies formed in the phorbol ester-treated group. Brief exposure (60 min) of cells to the phospholipase A2 inhibitors, mepacrine (500 mumol/l) and heparin (1 g/l), reduced the number of colonies formed in the control group and completely abolished the increase in the number of colonies formed after treatment of the cells with phorbol ester. When inhibitors of protein kinase C or phospholipase A2 were present during the entire period of the colony forming assay (7 days), no colonies could be scored in either the control or phorbol ester-treated groups of bone marrow cells. Long-term treatment or temporary exposure (60 min) of cells to indomethacin (50 mumol/l), an inhibitor of cyclooxygenase, or nordihydroguaiaretic acid (50 mumol/l), an inhibitor of lipoxygenase, had no effect on colony formation in both groups. Pretreatment of cells for 45 min with calcium ionophore A23187 (10 mumol/l) failed to increase the number of colonies, compared with the control group. Moreover, simultaneous treatment of cells for 45 min with phorbol ester (500 nmol/l) and A23187 (10 mumol) did not produce any further increase in the number of colonies, compared with the phorbol ester-treated group, suggesting that elevation of intracellular calcium is unimportant in the phorbol ester-mediated response. Dibutyryl cyclic adenosine monophosphate (50 mumol/l) in the presence or absence of phorbol ester, failed to stimulate colony formation, indicating that cyclic AMP-dependent protein kinases are not involved in the signalling process. Temporary exposure (75 min) of bone marrow cells to okadaic acid (1 mumol/l), a potent inhibitor of serine/threonine phosphatases, or to tyrphostine AG-115 (20 mumol/l), a tyrosine kinase inhibitor, did not effect colony growth in the control or phorbol ester-treated group. The results indicate that phospholipase A2 activation is involved in the phorbol ester-mediated increase in colony formation, since, of the different agents applied, only staurosporine, an inhibitor of protein kinase C, and mepacrine and heparin, putative inhibitors of phospholipase A2, were capable of abolishing phorbol ester-mediated effects.
Molecular Pathological Evaluation of Clusterin in a Rat Model of Unilateral Ureteral Obstruction as a Possible Biomarker of Nephrotoxicity

In the present study, to determine the validity of considering clusterin as a possible biomarker of nephrotoxicity, the expression and distribution of clusterin in the rat UUO kidney were investigated. Real-time RT-PCR revealed an immediate increase in the clusterin mRNA level in the kidney, within 6 hours after UUO, and also maintenance of the mRNA expression level from day-1 to day-3 was 60-fold higher in the UUO kidney than in the sham kidney. ISH analysis revealed clusterin mRNA signals in the UUO renal tubular epithelium, whereas no signal was observed in the sham kidney. Detection of clusterin-α and -β was conducted using the subtype-specific antibodies, by both of western blotting and immunohistochemistry. Although clusterin-α was predominant in the UUO urine, only faint signals were noted at the brush border of the tubular epithelium or intraductal. On the other hand, strong signals of clusterin-β were detected in the UUO kidney homogenate, and the molecule was localized in the renal tubular epithelium. These results suggest that clusterin was translated in the renal tubular epithelium after de novo expression induced by renal injury. Thus, detection of clusterin mRNA and clusterin-β in the kidney or clusterin-α in the urine may be useful for predicting nephrotoxicity.
NFAT2 inhibitor ameliorates diabetic nephropathy and podocyte injury in db/db mice

Podocyte injury plays a key role in the development of diabetic nephropathy (DN). We have recently shown that 11R‐VIVIT, an inhibitor of cell‐permeable nuclear factor of activated T‐cells (NFAT), attenuates podocyte apoptosis induced by high glucose in vitro. However, it is not known whether 11R‐VIVIT has a protective effect on DN, especially podocyte injury, under in vivo diabetic conditions. Hence, we examined the renoprotective effects of 11R‐VIVIT in diabetic db/db mice and the possible mechanisms underlying its protective effects on podocyte injury in vivo and in vitro.
Effect of a chronic high‐salt diet on whole‐body and organ sodium contents of Dahl rats

Objective To evaluate whether a high-salt diet causes retention of Na in Dahl rats. Design To compare the whole-body and organ (liver, spleen, kidney, heart, lung, femur, submaxillary gland and muscle) Na contents in Dahl salt-sensitive rats and Dahl salt-resistant rats. Methods Rats aged 6–10 weeks of both strains were fed a normal-salt (0.4% NaCl) or a high-salt (8% NaCl) diet. The whole-body and organs were then ashed and their respective Na contents determined. Results Salt-resistant rats fed the normal-salt diet had a higher whole-body Na content than did salt-sensitive rats. The high-salt diet increased the whole-body Na content of salt-sensitive rats significantly, but it did not increase that of salt-resistant rats. The high-salt diet caused a significant increase in the organ weight: body weight ratio for all organs of the salt-sensitive rats, except the submaxillary gland, but had no effect on the ratios for salt-resistant rats, apart from that for the kidney. The kidney, submaxillary gland and muscle Na concentrations were greater in salt-sensitive rats than they were in salt-resistant rats. Nonetheless, regardless of strain, the high-salt diet had no effect on organ and plasma Na concentrations. The high-salt diet increased the organ weights (liver, spleen, kidney, heart and lung) and the organ Na contents per kg body weight significantly for salt-sensitive rats but not for salt-resistant rats. Conclusions A high-salt diet caused Na retention in salt-sensitive rats only and this was partially due to enlargement of the organs.
Prenyl Alcohol Production by Expression of Exogenous Isopentenyl Diphosphate Isomerase and Farnesyl Diphosphate Synthase Genes in Escherichia coli

Isopentenyl diphosphate isomerase (idi) and farnesyl diphosphate synthase (ispA) genes were overexpressed in Escherichia coli. The resulting transformant showed 6.8-fold higher production of farnesol (389 μg/l). In a similar manner, overexpression of idi and mutated ispA led to high production of geranylgeraniol (128 μg/l).
ELECTROMAGNETIC TEMPERATURE EXTRAPOLATION IN DEPTH IN THE HENGILL GEOTHERMAL AREA , ICELAND

Indirect electromagnetic (EM) geothermometer developed recently in (Spichak et al., 2007a,b) is applied to the temperature extrapolation in depth in the Hengill geothermal zone (Iceland). The approach used is based on the artificial neural network (ANN) analysis of the implicit conductivity-temperature relations rather than on the prior assumptions of the electrical conductivity mechanisms. The samples for indirect EM geothermometer calibration consisted from the well temperature records and electrical conductivity values determined for the same depths from the magnetotelluric data measured in the vicinities of 8 boreholes. The testing of the estimates was carried out using the temperature records not involved in the calibration. The results indicate that the temperature extrapolation accuracy essentially depends on the ratio between the well length and the extrapolation depth. In particular, in extrapolation to a depth twice as large as the well depth the relative error is 5-6%, and in case of its threefold excess the error is around 20%. This result makes it possible to increase significantly the deepness of indirect temperature estimations in the geothermal areas without additional drilling. The method developed could be especially useful when exploring supercritical geothermal resources located at depths 4-5 km or deeper, where the temperature estimates could be made using the EM geothermometer calibrated by the shallow parts of the available temperature logs.
Streptococcal cysteine protease augments lung injury induced by products of group A streptococci

Streptococcus pyogenes infections in humans may be associated with severe clinical manifestations, including adult respiratory distress syndrome and a toxic shock-like syndrome. These observations have led to the investigation of products of group A streptococci that may contribute to increased virulence. Streptococcal pyrogenic exotoxin B is a highly conserved precursor of an extracellular cysteine protease that is secreted by S. pyogenes. We investigated the ability of this streptococcal cysteine protease (SCP) to act synergistically with either streptococcal cell wall antigen (SCW) or streptolysin-O (SLO) to augment lung injury in rats. Intratracheal administration of either SCW or SLO alone caused lung injury, as measured by pulmonary vascular leak. Bronchoalveolar lavage (BAL) fluid analysis showed that SCW induced neutrophil accumulation and appearance of interleukin-1beta and tumor necrosis factor alpha. In contrast, SLO induced neither neutrophil influx nor significant cytokine elevations in BAL fluids. Intratracheal administration of SCP with either SCW or SLO resulted in synergistic augmentation of lung vascular permeability and accumulation of BAL neutrophils. The synergy was reduced when SCP was either heat inactivated or coinstilled with a peptide inhibitor of the protease. SCP in the presence of SCW resulted in a significant increase in BAL fluid tumor necrosis factor alpha content but not in immunoreactive interleukin-1beta. Moreover, the copresence of SAP with SAW resulted in increased BAL fluid nitrite-nitrate levels, indicative of nitric oxide production. These data demonstrate that SCP acts synergistically with other S. pyogenes products (SCW or SLO) to increase tissue injury and provide additional evidence that SCP may function as an important virulence factor in group A streptococcal infections.
Role of bicarbonate in pH recovery from intracellular acidosis in the guinea‐pig ventricular myocyte.

1. Intracellular pH (pHi) was recorded ratiometrically in isolated guinea‐pig ventricular myocytes using the pH‐sensitive fluoroprobe, carboxy‐SNARF‐1 (carboxy‐seminaphthorhodafluor). 2. Following an intracellular acid load (10 mM NH4 Cl removal), pHi recovery in HEPES‐buffered Tyrode solution was inhibited by 1.5 mM amiloride (Na(+)‐H+ antiport blocker). In the presence of amiloride, switching from HEPES buffer to HCO3‐/CO2 (pHo of both solutions = 7.4) stimulated a pHi recovery towards more alkaline levels. 3. Amiloride‐resistant, HCO(3‐)‐dependent pHi recovery was inhibited by removal of external Na+ (replaced by N‐methyl‐D‐glucamine), whereas removal of external Cl‐ (replaced by glucuronate, leading to depletion of internal Cl‐), removal of external K+, or decreasing external Ca2+ by approximately tenfold had no inhibitory effect. These results suggest that the amiloride‐resistant recovery is due to a Na(+)‐HCO3‐ cotransport into the cell. 4. The stilbene derivative DIDS (4,4'‐diisothiocyanatostilbene‐2,2'‐disulphonic acid, 500 microM) slowed Na(+)‐HCO(3‐)‐dependent pHi recovery. 5. Intracellular pH increased in Cl(‐)‐free solution and this increase still occurred in Na(+)‐free solution indicating that it is not caused via Na(+)‐HCO3‐ symport and is more likely to be due to Cl‐ efflux in exchange for HCO3‐ influx on a sarcolemmal Cl(‐)‐HCO3‐ exchanger. The lack of any significant pHi recovery from intracellular acidosis in Na(+)‐free solution suggests that this exchanger does not contribute to acid‐equivalent extrusion. 6. Possible voltage sensitivity and electrogenicity of the co‐transport were examined by using the whole‐cell patch clamp technique in combination with SNARF‐1 recordings of pHi. Stepping the holding potential from ‐110 to ‐40 mV did not affect amiloride‐resistant pHi recovery from acidosis. Moreover, following an intracellular acid load, the activation of Na(+)‐HCO3‐ co‐influx (by switching from HEPES to HCO3‐/CO2 buffer) produced no detectable outward current (outward current would be expected if the coupling of HCO3‐ with Na+ were > 1.0). 7. Intracellular intrinsic buffering power (beta i) was assessed as a function of pHi (beta i computed from the decrease of pHi following reduction of extracellular NH4 Cl in amiloride‐containing solution). beta i in the ventricular myocyte increases roughly linearly with a decrease in pHi according the following equation: beta i = ‐28(pHi) +222.6. 8. Comparison of acid‐equivalent efflux via Na(+)‐HCO3‐ symport and Na(+)‐H+ antiport showed that, following an intracellular acidosis, the symport accounts for about 40% of total acid efflux, the other 60% being carried by the antiport. (ABSTRACT TRUNCATED AT 400 WORDS)
Migration and Economic Mobility in Tanzania: Evidence from a Tracking Survey

Abstract This study explores to what extent migration has contributed to improved living standards of individuals in Tanzania. Using a thirteen-year panel survey, we find that migration between 1991 and 2004 added 36 percentage points to consumption growth. Although moving out of agriculture resulted in much higher growth than staying in agriculture, growth was always greater in any sector if the individual physically moved. As to why more people do not move given the high returns to geographical mobility, analysis finds evidence consistent with models in which exit barriers set by home communities prevent the migration of some categories of people.
In vitro reversal of fragile‐X expression by exogenous thymidine

A virtually thymidine free medium was used to test the effects of exogenous thymidine on lymphocyte expression of the fragile‐X. De novo pathway thymidylic acid synthesis in the cells was blocked by FUdR. Our results suggest that in vitro exogenous thymidine is directly responsible for suppressing expression of the fragile‐X. More importantly, delayed addition of exogenous thymidine can negate fragile‐X expression after it has first been induced by FUdR.
Automatic design of IPMSMs using a GA coupled with the coarse-mesh finite element method

Interior permanent magnet synchronous motors (IPMSMs) are widely used in many applications because of their higher performance. In recent years, there has been an increasing interest in motor design technologies that can realize required specifications. Therefore, it is important to shorten the design period and generalize the design method. In the present paper, the design period is shortened using the coarse-mesh finite element method (FEM). The present paper demonstrates the usefulness of a genetic algorithm (GA) coupled with the coarse-mesh FEM for an IPMSM structure having a large high-efficiency operation area. As a result, the usefulness of the proposed method is confirmed, and a motor structure having a large high-efficiency operation area is obtained.
Glutamine reduces bacterial translocation after small bowel transplantation in cyclosporine-treated rats.

Bacterial translocation (BT) of enteric organisms is a major cause of sepsis in patients undergoing small bowel transplantation (SBT). Cyclosporine (CsA) may be toxic to intestinal epithelium and increase the risk of BT. Glutamine (Gln) is the preferred enterocyte fuel and maintains graft epithelial integrity in experimental SBT. This study determined the effects of CsA on mucosal structure and function of transplanted intestinal isograft and examined whether Gln-enriched diet reversed CsA-induced intestinal toxicity. Thirty-three adult Lewis rats underwent resection of the distal 60% of small bowel and received an orthotopic jejunal isograft. Rats received either elemental diet with 2% Gln or the same diet with balanced nonessential amino acids (non-Gln) by gastrostomy for 10 days. CsA (15 mg/kg, im) or olive oil was injected daily. Rats were assigned to four groups: non-Gln with vehicle, non-Gln with CsA, Gln with vehicle, and Gln with CsA. Mucosal villous height, surface area, crypt depth, 14C glucose absorption, BT to mesenteric lymph nodes (MLN), and body weight change were evaluated. The non-Gln with CsA group had the highest incidence of BT (P < 0.001). Gln groups had significantly decreased BT (P < 0.01) and increased crypt depth and villous surface area (P < 0.01) when compared to non-Gln groups. Body weight significantly decreased in CsA groups when compared to non-CsA groups (P < 0.01). These results indicate at CsA significantly decreased body weight and increased BT without decreasing mucosal structure and glucose absorption of intestinal isografts. (ABSTRACT TRUNCATED AT 250 WORDS)
Mutations in Plasmodium falciparum dihydrofolate reductase and dihydropteroate synthase and epidemiologic patterns of pyrimethamine-sulfadoxine use and resistance.

To assess the relationship between mutations in Plasmodium falciparum dihydrofolate reductase (DHFR) and dihydropteroate synthase (DHPS) and clinical pyrimethamine-sulfadoxine resistance, polymerase chain reaction surveys and analyses for new mutations were conducted in four countries with increasing levels of pyrimethamine-sulfadoxine resistance: Mali, Kenya, Malawi, and Bolivia. Prevalence of mutations at DHFR codon 108 and a new mutation at DHPS 540 correlated with increased pyrimethamine-sulfadoxine resistance (P < .05). Mutations at DHFR 51, DHFR 59, and DHPS 437 correlated with resistance without achieving statistical significance. Mutations at DHFR 164 and DHPS 581 were common in Bolivia, where pyrimethamine-sulfadoxine resistance is widespread, but absent in African sites. Two new DHFR mutations, a point mutation at codon 50 and an insert at codon 30, were found only in Bolivia. DHFR and DHPS mutations occur in a progressive, stepwise fashion. Identification of specific sets of mutations causing in vivo drug failure may lead to the development of molecular surveillance methods for pyrimethamine-sulfadoxine resistance.
Increasing Water Use Efficiency Comes at a Cost for Norway Spruce

Intrinsic water use efficiency (WUEi) in trees is an indication of the ratio of carbon assimilation to the rate of transpiration. It is generally assumed that it is a response to water availability. In agricultural research, the question of drought tolerance by increased WUEi has been well studied. In general, the increase is a trade-off for productivity and is therefore not desired. For forest trees, this question is less clearly understood. Using stable carbon isotopes derived from tree rings combined with productivity as the product of the annual growth increment and annual density measurements, we compared the change in WUEi over a 15 year period. While WUEi increased over this period, the productivity decreased, causing an opposing trend. The gradient of the correlation between WUEi and productivity varies between provenances and sites. Counterintuitively, the populations at the drier site showed low WUEi values at the beginning of the investigation. Slopes vary with the provenance from Poland showing the least decline in productivity. In general, we found that a decline in productivity aligned with an increase in WUEi.
Role of Neurotrophins in Diabetic Neuropathy and Treatment with Nerve Growth Factors

In rodent models of diabetes, there are expression deficits in nerve growth factor (NGF) and in mRNA for its high-affinity receptor, trkA, leading to decreased retrograde axonal transport of NGF and decreased support of NGF-dependent sensory neurons, with reduced expression of their neuropeptides, substance P and calcitonin gene-related peptide (CGRP). Treatment of diabetic rats with intensive insulin normalized these deficits, and treatment with exogenous NGF caused dose-related increases, giving levels of NGF and neuropeptides that were greater than those of controls. Neurotrophin-3 (NT-3) mRNA was also deficient in leg muscle from diabetic rats, and administration of recombinant NT-3 to diabetic rats increased the conduction velocity of sensory nerves without affecting motor conduction velocity. In regenerating nerves after experimental crush injury, expression of NGF in the nerve trunk is increased in diabetes to a greater extent than in controls, but this is offset by a greater reduction in the neuronal expression of trkA in dorsal root ganglia of diabetic rats. Nonetheless, targeted administration of exogenous NGF via impregnated conduits stimulated regeneration in both control and diabetic rats. These findings implicate deficient neurotrophic support in diabetic neuropathy and suggest that its correction should be a paramount therapeutic target.
Antioxidant Effect of Ethanolic Extract of Propolis in Liver of L-NAME Treated Rats.

BACKGROUND The blocking of nitric oxide synthase (NOS) activity may cause vasoconstriction with formation of reactive oxygen species. Propolis is a natural product collected from plants by honeybees. Propolis has biological and pharmacological properties. OBJECTIVES This study was designed to investigate the effects of propolis on catalase (CAT) activity, nitric oxide (NO) and malondialdehyde (MDA) levels in the liver tissues of NOS inhibited rats by Nω-Nitro-L-arginine methyl ester (L-NAME). MATERIAL AND METHODS Rats were given a NOS inhibitor (L-NAME, 40 mg/kg, intraperitoneally) for 15 days to provoke hypertension and propolis (200 mg/kg, by gavage) the last 5 of the 15 days. RESULTS Nitric oxide levels in the liver tissue of the rats given L-NAME significantly decreased (p<0.01). That parameter did not significantly alter in the liver of rats treated with propolis compared to the control group. CAT activity and MDA levels in the liver of the rats administrated L-NAME significantly increased compared to the control group (p<0.01). These parameters significantly decreased in the liver of the rats given L-NAME + propolis compared to the L-NAME group (p<0.01). CONCLUSIONS The present data shows that L-NAME in the liver may enhance oxidative stress via inhibited nitric oxide synthase. Our results also suggest that this effect is suppressed by the antioxidant properties of propolis in the liver tissue of NOS inhibited rats.
A NEW TECHNIQUE FOR MITIGATION OF TRANSFORMER INRUSH CURRENT

Transformer inrush currents are high-magnitude, harmonic-rich currents generated when transformer cores are driven into saturation at the time of switching-on. These have an adverse effect on the security and stability of the power system. In this paper, a new simple and efficient technique for inrush current reduction is proposed. It is based on core flux reduction prior to primary circuit energization. Flux reduction can be achieved by applying a voltage to the core with the help of a tertiary winding. The effectiveness of the proposed technique is established through both computer simulation using PSCAD and laboratory experiments. The investigations indicate that the method reduces the magnetization inrush currents significantly.
Impaired paracellular ion transport in the loop of Henle causes familial hypomagnesemia with hypercalciuria and nephrocalcinosis

Familial hypomagnesemia with hypercalciuria and nephrocalcinosis (FHHNC) is a rare tubular disorder caused by mutations in genes coding for tight junction (TJ) proteins. TJs define the paracellular path between adjacent cells and thereby play a pivotal role for the regulation of the paracellular ion permeability of epithelia. The family of TJ proteins comprise a variety of transmembrane proteins, including the claudins. Multiple distinct mutations in the genes for claudin‐16 and ‐19 have been described to be responsible for FHHNC. Both encoded proteins are especially important for the paracellular reabsorption of Mg2+ and Ca2+ in the thick ascending limb of Henle's loop. Interestingly, in addition to ion disturbances, FHHNC leads to chronic renal failure and may be associated with extrarenal symptoms.