Gotowe bibliografie tematyczne / Acidosis

Gotowa bibliografia na temat „Acidosis”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 30 lipca 2024

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Artykuły w czasopismach na temat "Acidosis"

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Areas, Jorge, Sevag Balian, Dianna Slemmer, Mario Belledonne i Harry G. Preuss. "Renal ammoniagenesis following glutamine loading in intact dogs during acute metabolic acid–base perturbations". Clinical Science 72, nr 1 (1.01.1987): 61–69. http://dx.doi.org/10.1042/cs0720061.

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1. Adaptation of renal ammoniagenesis during acute metabolic acidosis in intact dogs may be nonexistent or, at least, markedly less than in chronic acidosis. This contrasts to adaptation in acute respiratory acidosis, where levels similar to those attained in chronic acidosis occur within hours. 2. Accordingly, the inability to discern marked changes in acute metabolic acidosis compared with acute respiratory acidosis has been attributed to decreased glomerular filtration rate and renal blood flow seen frequently in the former. 3. In our studies, we found early changes in ammoniagenesis and glutamine metabolism during acute metabolic acidosis, but not of the magnitude seen in chronic acidosis, even considering the changes in renal blood flow (RBF) and glomerular filtration rate (GFR). Exogenous glutamine loading allowed us to discover that the qualitative changes in glutamine metabolism during acute metabolic acidosis differed from control but fell short of those seen in chronic metabolic a acidosis. 4. We also examined glutamine metabolism when renal ammoniagenic adaptation was acutely inhibited in chronically acidotic dogs. Infusing NaHCO3 into chronically acidotic dogs decreased renal ammonia production significantly (247 μmol min−1 100 ml−1 GFR vs 148 μmol min−1 100 ml−1 GFR: P < 0.001) and glutamine extraction (111.8 μmol min−1 100 ml−1 GFR vs 90.9 μmol min−1 100 ml−1 GFR: P < 0.02). 5. The qualitative changes in renal glutamine metabolism in both studies suggest that alterations in deamination of glutamate formed from glutamine are responsible, at least in part, for adaptation to acute acid–base perturbations. 6. Compared with respiratory acidosis, adaptation to metabolic acidosis is progressive and prolonged.
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Williams, Bryan, Ellis Layward i John Walls. "Skeletal muscle degradation and nitrogen wasting in rats with chronic metabolic acidosis". Clinical Science 80, nr 5 (1.05.1991): 457–62. http://dx.doi.org/10.1042/cs0800457.

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1. Chronic metabolic acidosis is associated with impaired growth and negative nitrogen balance, suggesting that it promotes endogenous protein catabolism. 2. Skeletal muscle is the major repository of body protein and is a potential target for stimuli of protein catabolism. 3. This study in vivo examines the effects of chronic metabolic acidosis on the relationship between growth, nitrogen disposal and skeletal muscle catabolism in the rat. 4. Growth, nitrogen utilization and acquisition of body mass were significantly impaired in acidotic animals compared with pair-fed controls. 5. Total nitrogen excretion was significantly increased in acidotic rats despite decreased urea production. The time course of this response to acidosis was synchronous with that of accelerated protein catabolism in skeletal muscle. 6. It is proposed that metabolic acidosis impairs growth by stimulating skeletal muscle protein catabolism. It is suggested that this forms part of a co-ordinated multi-organ homoeostatic response to acidosis, skeletal muscle and down-regulated urea production supplying the nitrogen required for renal ammoniagenesis.
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Challa, A., R. J. Krieg, M. A. Thabet, J. D. Veldhuis i J. C. Chan. "Metabolic acidosis inhibits growth hormone secretion in rats: mechanism of growth retardation". American Journal of Physiology-Endocrinology and Metabolism 265, nr 4 (1.10.1993): E547—E553. http://dx.doi.org/10.1152/ajpendo.1993.265.4.e547.

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To test the hypothesis that growth retardation in nonanion gap acidosis may be associated with impairment of growth hormone (GH) secretory patterns, we examined GH secretion in rats made acidotic with ammonium chloride ingestion. Considerable growth retardation was demonstrated in pair-fed and acidotic rats after 1 wk of ammonium chloride ingestion compared with control. With stable metabolic acidosis sustained on the 8th day of experiment, pulsatile secretion of GH was evaluated by blood samples drawn every 10 min for 6 h. Using deconvolution analysis to quantitate in vivo GH secretory rates, we found significant inhibition of pulsatile GH secretion in acidotic rats. Changes in amplitude of GH pulses and mean mass of GH pulses correlated with changes in body weight. These studies showed that chronic metabolic acidosis causes growth impairment, reduced food efficiency, and amplitude-specific inhibition of pulsatile secretion of GH. We propose that this GH axis suppression, whether mediated by decreased nutrients or not, contributes significantly to growth failure in children with renal tubular acidosis. Because a similar degree of inhibition of GH secretion was seen in pair-fed rats, we infer that insufficient calorie intake in metabolic acidosis may contribute to disruption of normal GH secretion patterns. These changes in GH secretion were specific, because acidotic rats were different from pair-fed controls in that they showed no change in either half-life of GH in circulation or in pulse frequency. Such observations offer a rationale for more detailed clinical investigations into the impact of metabolic acidosis on physiological regulation of pulsatile GH secretion in humans.
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Moody, Mikayla, Tannin A. Schmidt, Ruchir Trivedi i Alix Deymier. "Administration of alendronate exacerbates ammonium chloride-induced acidosis in mice". PLOS ONE 18, nr 9 (15.09.2023): e0291649. http://dx.doi.org/10.1371/journal.pone.0291649.

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Bone disease is highly prevalent in patients with chronic kidney disease (CKD), leading to an increased risk of bone fractures. This is due in part to metabolic acid-induced bone dissolution. Bisphosphonates (BPPs) are a potential treatment for inhibiting bone dissolution; however, there are limited studies observing the use of BPPs on acidotic patients. We aimed to determine efficacy of BPPs on maintaining bone health and pH regulation in acid-exposed mice. Using a diet-induced murine model of metabolic acidosis, we examined bone structure, composition, and mechanics as well as blood gases for three groups: control, acidosis, and acidosis + bisphosphonates (acidosis+BPP). Acidosis was induced for 14 days and alendronate was administered every 3 days for the acidosis+BPP group. The administration of BPP had little to no effect on bone structure, mechanics, and composition of the acidosis bones. However, administration of BPP did cause the mice to develop more severe acidosis than the acidosis only group. Overall, we discovered that BPPs may exacerbate acidosis symptoms by inhibiting the release of buffering ions from bone. Therefore, we propose that BPP administration should be carefully considered for those with CKD and that alkali supplementation could help minimize acidifying effects.
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Caso, Giuseppe, Barbara A. Garlick, George A. Casella, Dawn Sasvary i Peter J. Garlick. "Acute metabolic acidosis inhibits muscle protein synthesis in rats". American Journal of Physiology-Endocrinology and Metabolism 287, nr 1 (lipiec 2004): E90—E96. http://dx.doi.org/10.1152/ajpendo.00387.2003.

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In this study, we investigated the effect of acute metabolic acidosis on tissue protein synthesis. Groups of rats were made acidotic with intragastric administration of NH4Cl (20 mmol/kg body wt every 12 h for 24 h) or given equimolar amounts of NaCl (controls). Protein synthesis in skeletal muscle and a variety of different tissues, including lymphocytes, was measured after 24 h by injection of l-[2H5]phenylalanine (150 μmol/100 g body wt, 40 moles percent). Results show that acute acidosis inhibits protein synthesis in skeletal muscle (−29% in gastrocnemius, −23% in plantaris, and −17% in soleus muscles, P < 0.01) but does not affect protein synthesis in heart, liver, gut, kidney, and spleen. Protein synthesis in lymphocytes is also reduced by acidosis (−8%, P < 0.05). In a separate experiment, protein synthesis was also measured in acidotic and control rats by a constant infusion of l-[2H5]phenylalanine (1 μmol·100 g body wt−1·h−1). The results confirm the earlier findings showing an inhibition of protein synthesis in gastrocnemius (−28%, P < 0.01) and plantaris (−19%, P < 0.01) muscles but no effect on heart and liver by acidosis. Similar results were also observed using a different model of acute metabolic acidosis, in which rats were given a cation exchange resin in the H+ (acidotic) or the Na+ (controls) form. In conclusion, this study demonstrates that acute metabolic acidosis for 24 h depresses protein synthesis in skeletal muscle and lymphocytes but does not alter protein synthesis in visceral tissues. Inhibition of muscle protein synthesis might be another mechanism contributing to the loss of muscle tissue observed in acidosis.
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TETA, Daniel, Alan BEVINGTON, Jeremy BROWN, David THROSSELL, Kevin P. G. HARRIS i John WALLS. "Effects of acidosis on leptin secretion from 3T3-L1 adipocytes and on serum leptin in the uraemic rat". Clinical Science 97, nr 3 (6.08.1999): 363–68. http://dx.doi.org/10.1042/cs0970363.

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Marked hyperleptinaemia and metabolic acidosis are common findings in patients with chronic renal failure. In animal models, both leptin administration and acidosis reduce food intake. However, leptin causes loss of body fat, while acidosis induces muscle wasting. Whether a low pH and leptin production are related has not been studied. Leptin secretion was measured in cultured 3T3-L1 adipocytes exposed to acid or control pH for up to 96 h. In addition, serum leptin was compared between acidotic and bicarbonate-treated uraemic Wistar rats using the remnant model. Leptin levels in the culture medium were decreased at an acid pH of 7.1 compared with a control pH of 7.5 at 96 h (562±78 and 831±103 pg·48 h-1·well-1 respectively; mean±S.E.M.; P = 0.037). Similarly, serum leptin in uraemic rats was found to be lower in the acidotic group than in the bicarbonate-treated group, although this observation fell just short of statistical significance (1273±171 compared with 2059±376 pg/ml; P = 0.07). In conclusion, acidosis decreases leptin secretion from cultured adipocytes. Accordingly, acidotic uraemic rats seem to exhibit lower serum leptin levels than their bicarbonate-supplemented counterparts. This study is the first report providing a link between acidosis and leptin levels.
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7

Türe, Hatice, Özgül Keskin, Ülkem Çakır, Canan Aykut Bingöl i Uğur Türe. "The frequency and severity of metabolic acidosis related to topiramate". Journal of International Medical Research 44, nr 6 (27.10.2016): 1376–80. http://dx.doi.org/10.1177/0300060516669897.

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Objective We planned a cross-sectional analysis to determine the frequency and severity of metabolic acidosis in patients taking topiramate while awaiting craniotomy. Methods Eighty patients (18 – 65 years) taking topiramate to control seizures while awaiting elective craniotomy were enrolled. Any signs of metabolic acidosis or topiramate-related side effects were investigated. Blood chemistry levels and arterial blood gases, including lactate, were obtained. The severity of metabolic acidosis was defined according to base excess levels as mild or moderate. Results Blood gas analysis showed that 71% ( n = 57) of patients had metabolic acidosis. The frequency of moderate metabolic acidosis was 56% ( n = 45), while that of mild metabolic acidosis was 15% ( n = 12). A high respiratory rate was reported in only 10% of moderately acidotic patients. Conclusions In patients receiving topiramate, baseline blood gas analysis should be performed preoperatively to determine the presence and severity of metabolic acidosis.
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Price, S. R., X. Wang i J. L. Bailey. "Tissue-specific responses of branched-chain alpha-ketoacid dehydrogenase activity in metabolic acidosis." Journal of the American Society of Nephrology 9, nr 10 (październik 1998): 1892–98. http://dx.doi.org/10.1681/asn.v9101892.

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In adrenalectomized rats, acidosis does not increase whole-body leucine oxidation unless a physiologic amount of glucocorticoids (dexamethasone) is also provided; an equivalent dose of dexamethasone without acidosis does not change leucine catabolism. Because the influences of acidification and glucocorticoids on branched-chain amino acid metabolism in specific organs are unknown, the function of branched-chain alpha-ketoacid dehydrogenase (BCKAD), the rate-limiting enzyme in branched-chain amino acid catabolism, in adrenalectomized rat skeletal muscle and liver, the two major tissues that degrade branched-chain amino acid was measured. In muscle of acidotic adrenalectomized rats receiving dexamethasone, basal and total BCKAD activities were increased 2.6- (P < 0.05) and 2.8-fold (P < 0.05), respectively. Neither acidosis nor dexamethasone alone increased these activities. BCKAD E1alpha subunit mRNA in muscle of acidotic rats given dexamethasone was increased 1.89-fold (P < 0.05) in parallel with the change in BCKAD activity; BCKAD E2 subunit mRNA was increased by acidosis, dexamethasone, or a combination of both stimuli. In contrast, basal BCKAD activity in liver of rats with acidosis or dexamethasone was nearly threefold lower (P < 0.05) and changes in enzyme activity reflected reduced subunit mRNA. Thus, there are reciprocal, tissue-specific changes in BCKAD function in response to acidosis.
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Karinch, Anne M., Cheng-Mao Lin, Christopher L. Wolfgang, Ming Pan i Wiley W. Souba. "Regulation of expression of the SN1 transporter during renal adaptation to chronic metabolic acidosis in rats". American Journal of Physiology-Renal Physiology 283, nr 5 (1.11.2002): F1011—F1019. http://dx.doi.org/10.1152/ajprenal.00106.2002.

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During chronic metabolic acidosis, renal glutamine utilization increases markedly. We studied the expression of the system N1 (SN1) amino acid transporter in the kidney during chronic ammonium chloride acidosis in rats. Acidosis caused a 10-fold increase in whole kidney SN1 mRNA level and a 100-fold increase in the cortex. Acidosis increased Na+-dependent glutamine uptake into basolateral and brush-border membrane vesicles (BLMV and BBMV, respectively) isolated from rat cortex (BLMV, 219 ± 66 control vs. 651 ± 180 pmol · mg−1 · min−1 acidosis; BBMV, 1,112 ± 189 control vs. 1,652 ± 148 pmol · mg−1 · min−1 acidosis, both P < 0.05). Na+-independent uptake was unchanged by acidosis in BLMV and BBMV. The acidosis-induced increase in Na+-dependent glutamine uptake was eliminated by histidine, confirming transport by system N. SN1 protein was detected only in BLMV and BBMV from acidotic rats. After recovery from acidosis, SN1 mRNA and protein and Na+-dependent glutamine uptake activity rapidly returned to control levels. These data provide evidence that regulation of expression of the SN1 amino acid transporter is part of the renal homeostatic response to acid-base imbalance.
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Lucioni, Alvaro, Christopher Womack, Mark W. Musch, Flavio L. Rocha, Cres Bookstein i Eugene B. Chang. "Metabolic acidosis in rats increases intestinal NHE2 and NHE3 expression and function". American Journal of Physiology-Gastrointestinal and Liver Physiology 283, nr 1 (1.07.2002): G51—G56. http://dx.doi.org/10.1152/ajpgi.00529.2001.

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Chronic metabolic acidosis increases intestinal Na absorption, although through undefined mechanisms. Whether this occurs through enhanced expression and/or function of the brush-border Na+/H+ exchangers (NHE)2 and NHE3 is unknown. Metabolic acidosis was induced in rats by feeding ammonium chloride through their drinking water. Intestinal NHE activities were measured using brush-border 22Na+ uptake. Western and Northern blots measured changes in protein and mRNA expression, respectively. Acidosis occurred within 2 days of ammonium chloride feedings but increased after 6 days. NHE2 and NHE3 activities, protein expression, and mRNA levels increased in acidotic rats compared with controls. In contrast, basolateral NHE1 expression was not affected. Brush-border alkaline phosphatase showed no effect of metabolic acidosis on cellular differentiation. This study demonstrated a direct effect of metabolic acidosis on NHE2 and NHE3 activity, expression, and gene transcription. Metabolic acidosis is one of the few circumstances shown to affect NHE2 function and expression, thus providing insights into the role of NHE2 on intestinal physiology.
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Rozprawy doktorskie na temat "Acidosis"

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Force, Lisa Marie. "Traumatic brain injury and acidosis /". view abstract or download text of file, 2006. http://hdl.handle.net/1794/3913.

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Maruta, Celso Akio. "Comparação da susceptibilidade de bovinos das raças Jersey e Gir à acidose láctica ruminal, induzida experimentalmente com sacarose". Universidade de São Paulo, 2000. http://www.teses.usp.br/teses/disponiveis/10/10136/tde-24072007-082404/.

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Foram utilizados neste experimento quatro garrotes Jersey (J) e quatro Gir (G), providos de cânula ruminal. Dois meses antes da indução da acidose láctica ruminal (ALR), os animais foram alimentados com dieta padronizada a base de feno e concentrado. A ALR foi induzida experimentalmente por meio da administração de sacarose intraruminal, correspondente ao peso metabólico corrigido, segundo técnica descrita por ORTOLANI (l995). Colheitas de sangue, suco de rúmen, urina, fezes e exames clínicos foram realizados nos seguintes momentos após a indução: zero, 14, 16, 18, 20, 22 e 24 horas. O pH e as concentrações de ácido láctico total, D e L e de seus sais foram determinados em todos os materiais biológicos colhidos. No sangue foram avaliados o hematócrito, os exames gasométricos e a concentração de creatinina; esta última substância também foi determinada na urina. Após a última colheita, todo o conteúdo ruminal foi completamente retirado para a determinaçãodo seu volume. Os bovinos de ambas as raças apresentaram marcante e idêntica acidose ruminal, não ocorrendo diferença no pH e na concentração de ácido láctico total, L e D no suco de rúmen. A acidose metabólica sistêmica foi moderada em ambas as raças, porém esta foi mais intensa nos bovinos J, confirmada pelas menores concentrações médias de bicarbonato e TCO2 (P < 0,00001) e pelo menor pH sangüíneo, (p < 0,025). Os garrotes J absorveram maiores quantidades de ácido láctico total e do isômero D; este último apresentou correlação negativa com o pH sangüíneo nesta raça (r = -O,78). Os garrotes G apresentaram maior capacidade homeostática de manutenção de pH sangüíneo no final da indução, provavelmente pela maior metabolização do lactato-L. Entretanto, os mesmos animais tiveram maior grau de desidratação, evidenciado pelas maiores porcentagens de hematócrito e de déficit de volume plasmático (p < 0,00001). Nessa raça ocorreu uma menor filtração glomerular, demonstrada pela maior concentração sérica de creatinina (p < 0,00001), menor depuração deste catabólito (p < 0,003) e menor volume urinário estimado (p < 0,05). Não ocorreram diferenças significativas no pH fecal entre as raças estudadas. Houve correlação negativa entre a concentração de lactato total fecal e o correspondente pH (r = - 0,65).
Four Jersey (J) and four Gir (G) rumen-cannulated steers were used. The steers were fed, for two months before the beginning of the rumen lactic acidosis (RLA) induction, a standard diet of hay and concentrates. The RLA was induced experimentally through the administration of sucrose into the rumen, according to the corrected metabolic weight, after ORTOLANI (1995). Blood, rumen fluid, urine, and fecal samples were collected and clinical examination carried out in the following times after the induction: zero, 14, 16, 18, 20, 22 and 24 hours. The pH, the total lactic acid and its L and D isomers were determined in all samples. The hematocrit, acid-base variables and the creatinine concentration were determined in the blood samples; creatinine was also determined in the urine samples. All the rumen content was evacuated in order to evaluate its volume at the 24th h. A intense rumen acidosis was reached; no differences in the rumen fluid pH and in the concentration of the total lactic acid and its isomers were found in both studied breeds. A moderate level of systemic metabolic acidosis was reached in both breeds, but lower overall mean of bicarbonate and TCO2 (p < 0.0001) as well as blood pH (p < 0.025) were found in the J steers. These steers absorbed higher amounts of total lactic and its D isomer than the G animals; the higher the blood D-lactate concentration, the lower the blood pH (r = - O.78) in the former breed. Better blood pH homeostasis were kept, at the end of induction, by the G steers, probably by their higher efficiency to metabolize L-lactate. However, the G steers exhibited a higher level of dehydration as seen by the greater hematocrit and plasma volume deficit (p < 0.00001). They also presented a lower glomerular filtration as evidenced by the higher creatinine serum levels (p < 0.00001), its lower urinary clearance (p < 0.003) and the lower estimated urinary volume (p < 0.05). There were no differences in the fecal pH values presented by both breeds. There was a negative correlation between the fecal total lactate concentration and the fecal pH (r = - 0.65).
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Pinto, Ana Carolina Janssen. "Adaptação a dietas de alta energia para bovinos Nelore submetidos previamente à restrição nutricional ou consumo de concentrados e efeitos nas características ruminais". Universidade Estadual Paulista (UNESP), 2017. http://hdl.handle.net/11449/152743.

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O objetivo deste estudo foi avaliar o efeito da restrição alimentar prévia ou exposição anterior a ingredientes concentrados sobre o tempo para adaptação à dietas de alto concentrado, sob os parâmetros da fermentação ruminal e o perfil de microrganismos ruminais de bovinos Nelore canulados confinados. Foram utilizados 6 bovinos da raça Nelore, castrados, com peso vivo inicial aproximado de 236 ± 23 kg, 15 meses de idade e canulados no rúmen, os quais foram divididos em dois quadrados latinos 3 x 3. Os tratamentos diferiram somente sobre o tipo de alimentação estabelecida previamente ao período de adaptação: Controle (forragem ad libitum + suplemento mineral); Restrição (forragem restrita a 1,4% do peso vivo + suplemento mineral) e Concentrado (forragem ad libitum + 0,5% do peso vivo de ingredientes concentrados e suplemento mineral). A duração deste estudo foi de 119 dias, sendo compostos por 3 períodos experimentais (33 dias cada período) e dois intervalos de washout (10 dias) entre os períodos 1 e 2, e 2 e 3. Os períodos foram divididos em: 14 dias de pré- adaptação, 6 dias de adaptação 1 (72% de concentrado), 6 dias de adaptação 2 (79% de concentrado) e 7 dias de dieta de terminação (86% de concentrado). O pH ruminal foi monitorado por meio da utilização de data loggers a cada 10 minutos. Foram avaliados a concentração de ácidos graxos de cadeia curta e amônia ruminal; a quantificação relativa das bactérias celulolíticas e utilizadoras de lactato por meio da técnica de PCR e a contabilidade total e diferencial de protozoários (0,4,8 e 12 horas após o trato). Os animais restritos, na fase de adaptação, tiveram maior concentração de AGCC (P< 0,01), maior duração de pH abaixo de 6,2 (P<0,01) e menor pH máximo nos dias 15 e 16 (P≤ 0,10) em relação ao tratamento controle. Na fase de terminação, esses animais tiveram menor CMS (P=0,02), maior pH médio e menor área de pH abaixo de 6,2 (P≤0,10) em relação ao tratamento controle. Os animais expostos previamente ao concentrado, na fase de adaptação, tiveram menor concentração de butirato e NH3 ruminal (P≤0,10) em relação ao tratamento controle. Apresentaram também menor quantidade relativa de Fibrobacter succinogenes (P=0,10) e maior CMS (P<0,01) em relação ao controle. Já na fase de terminação o CMS não teve diferença significativa em relação ao tratamento controle. Os animais que passaram por restrição alimentar ou por exposição de concentrado na fase de pré-adaptação apresentam características ruminais semelhantes durante a fase a terminação aos animais em forragem ad libitum.
The objective of this study was to evaluate the effect of diet restriction or prior exposure to concentrate ingredientes prior to the adaption period to high concentrate diet on parameters ruminal fermentation patterns and ruminal microorganisms profile of cannulated Nellore cattle. Six Nelore steers was used, with initial body weight about 350 kg, 20 months and cannulated in the rumen, which will be divided into two Latin squares 3 x 3. The treatments differed only with respect to the type of diets prior to the adaptation period: Control (forage ad libitum + mineral supplement); Restriction (forage restricted to 1.4% of body weight + mineral supplement) and concentrate (forage ad libitum + 0.5% of the body weight of concentrated ingredients + mineral supplement). The study was last 119 days, in which animals was submitted to three experimental periods (33 days each one) and two washout intervals (10 days) between the periods 1 and 2, 2 and 3; each period was divided as follows: 14 days of pre-adaptation, 6 days of adaptation 1 (72% concentrate), 6 days of adaptation 2 (79% concentrate) and 7 days of finishing diet (88% concentrate). The rumen pH and temperature was be monitored through the use of data loggers it was evaluated the rumen production of short chain fatty acids and ammonia concentration; the relative quantification of cellulolytic, amylolytic and lactate bacteria utilizing PCR and total and differential quantification of protozoa. Thus, the hypothesis is to test if Nelore cattle exposed to feed restriction or comsuption of concentrate ingredientes prior to the adaptation period present same rumen fermentation patters and microrganism profile when compared to animals of control treatment in the finish diet. Restricted animals, in the adaptation phase, had a higher concentration of SCFA (P<0.01), a higher duration of pH below 6.2 (P <0.01) and lower maximum pH on days 15 and 16 (P≤ 0.10) in relation to the control treatment. In the finish diet, these animals had lower DMI (P = 0.02), higher mean pH and lower pH area below 6.2 (P≤0.10) in relation to the control treatment. The animals previously exposed to the concentrate in the adaptation diet had a lower concentration of butyrate and ruminal NH3 (P≤0.10) in relation to the control treatment. They also presented lower amount of Fibrobacter succinogenes (P = 0.10) and higher DMI (P <0.01) in relation to the control. In the termination diet the DMI did not affect in relation to the control treatment. Cattle previously submitted to either nutricional restriction or intake of concentrate have similar ruminal characteristics during the finishing diet of the animals in control treatment.
2016/04262-8
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Vivan, Maria Carolina Ribeiro [UNESP]. "Correlação dos níveis de lactato sanguíneo com o estado neurológico e cardiorrespiratório de filhotes de cães nascidos de parto normal ou cesariana sob anestesia geral inalatória". Universidade Estadual Paulista (UNESP), 2010. http://hdl.handle.net/11449/92186.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
A avaliação da perfusão tecidual com macroparâmetros não permite a detecção precoce de alteração na microvasculatura. A anestesia da gestante requer avaliação da perfusão e a eficácia do lactato na identificação de complicações em crianças após o parto já foi descrita. O presente estudo objetivou validar o lactato sanguíneo e correlacioná-lo a métodos, na avaliação de neonatos de parto normal ou cesariana eletiva sob anestesia geral inalatória. Foram utilizadas oito cadelas para realização de parto normal ou cesariana eletiva, com o protocolo composto de morfina, propofol e sevofluorano. Foram avaliados 24 neonatos de parto normal (GN) e 30 de cesariana (GC), com exames de sangue umbilical no nascimento para dosagem de lactato, hemogasometria, hematócrito, glicose e eletrólitos. No nascimento e aos 10 minutos de vida foram realizadas avaliações Apgar e neurológica. O lactato foi avaliado aos 10 minutos, 4 e 30 dias de vida. Os filhotes apresentaram acidose respiratória, acidemia e hipoxemia ao nascimento, mais elevada no GC. Os animais do GC apresentaram notas de Apgar e resposta neurológica menores ao nascimento, com melhora aos 10 minutos. O lactato sanguíneo foi maior nos animais do GN no nascimento, e foi maior nos animais que morreram. A correlação entre o lactato e as variáveis ocorreu em GN. O lactato sanguíneo associado aos demais parâmetros foi útil na avaliação dos neonatos do GN, porém nos animais do GC não houve correlação com a condição clínica dos animais no momento do nascimento. O procedimento anestésico influencia nos valores de lactato, e a determinação do melhor intervalo para sua avaliação nesses pacientes é necessária.
The assessment of tissue perfusion using macro parameters does not allow early detection of changes in the microvasculature. Anesthesia for pregnant patient requires evaluation of perfusion, and the lactate effectiveness in identifying complications in children after birth has been described. This study aimed to validate the blood lactate and its correlation with other methods, in the evaluation of neonates born from vaginal delivery or elective cesarean section under inhalator anesthesia. Eight dogs were used to perform normal delivery or cesarean section, with the protocol consisting of morphine, propofol and sevoflurane. At birth were evaluated 24 neonates born from vaginal delivery (NG) and 30 born from cesarean section (CG) using umbilical blood to test lactate, blood gas, hematocrit, glucose and electrolytes. Apgar score and neurologic tests were performed at birth and at 10 minutes of life. Lactate levels were evaluated at 10 minutes, 4 and 30 days of life. The puppies showed respiratory acidosis, hypoxemia and acidemia at birth, higher in the CG. The animals of CG presented lower Apgar scores and neurological response at birth, which improved in 10 minutes. Blood lactate was higher in NG animals at birth, and was higher in those who died. The correlation between lactate and the variables occurred on NG. Association of blood lactate with other parameters was useful in the evaluation of neonates on NG, but in the animals of CG there was no correlation with the clinical condition of animals at birth. Anesthesia influences the lactate values, and it is necessary to determine the best interval for evaluation in these patients.
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Pereira, Ismael de Castro. "Estudo meta-analítico da flutuação de ingestão de massa seca no desempenho, comportamento ingestivo e saúde ruminal de bovinos confinados com dietas de alto concentrado". Botucatu, 2016. http://hdl.handle.net/11449/141503.

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Orientador: Mário De Beni Arrigoni
Resumo: O presente estudo teve o objetivo de avaliar o impacto da flutuação natural da ingestão de massa seca no desempenho, características de carcaça, comportamento ingestivo, perfil metabólico sanguíneo e aspectos morfofisiológicos ruminais de bovinos alimentados com dietas de alta inclusão de concentrado, por meio de estudo meta-analítico. Os experimentos contidos na meta-análise utilizaram animais com grupamento genético similar ao utilizado em confinamentos comerciais brasileiros. A meta-análise teve como base de dados os resultados de dez experimentos conduzidos no Confinamento Experimental da Faculdade de Medicina Veterinária e Zootecnia da UNESP, em Botucatu, entre os anos de 2006 e 2015. Os dados foram coletados a partir 838 bovinos, divididos em 238 baias, consideradas as unidades experimentais para o estudo. Os valores de flutuação de ingestão de massa seca na baia foram calculados pela diferença da ingestão de massa seca entre dois dias consecutivos e dividido pelo dia anterior para encontrar o valor em porcentagem. Com base na mediana geral de 5,62%, os animais foram divididos em dois grupos: alta e baixa flutuação de massa seca. As análises estatísticas foram feitas com auxílio do programa computacional R (versão 3.2.3). Utilizou-se um modelo de regressão linear misto para analisar os dados, no qual os experimentos e baias foram considerados como variáveis aleatórias e grupos de flutuação como variável fixa. Os grupos de baixa e alta flutuação apresentaram flutuação mé... (Resumo completo, clicar acesso eletrônico abaixo)
Abstract: This study aimed to evaluate the inpact of natural dry matter intake fluctuation on performance, carcass characteristics, feeding behavior, blood metabolic profile and morphophysiological ruminal aspects of cattle fed with diets of high inclusion of concentrate. The experiments used for this meta-analysis used cattle with genetic group similar to used in Brazilian commercial feedlots. The meta-analysis was conducted using a database of results of ten experiments conducted in Experimental Feedlot of Faculty of Veterinary Medicine and Animal Science, UNESP, Botucatu, between the years 2006 and 2015. Data were collected from 838 bulls, divided into 238 pens, considered the experimental units for the study. The values of dry matter intake fluctuation were calculated by the difference in dry matter intake between consecutive days and divided by the previous day to find the value in percentage. Based on the overall median of 5.62% cattle were classified into two groups: high- or low-fluctuation. All data analysis was performed in R using a mixed model approach where pens and year were random variables and fluctuation group fixed. The low and high fluctuation groups presented a dry matter intake fluctuation average of 4.79% and 6.74%, respectively. Low fluctuation group showed higher dry matter intake as percent of body weight (P <0.01), higher average daily gain (P = 0.05), higher dry matter intake in kg (P = 0.06), greater total weight gain (P = 0.08), as well as greater depositio... (Complete abstract click electronic access below)
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Bethell, H. W. L. "Potassium, acidosis and ventricular repolarisation during ischaemia". Thesis, University of Cambridge, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596607.

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In the first section the relative severity of the insult produced by low-flow ischaemia was established through a series of experiments monitoring the change in intracellular pH, high energy phosphates and LVDP during zero-flow, low flow (7.5% of the control flow rate) and moderate flow ischaemia (30% of the control flow rate). This established that in terms of mechanical performance and bioenergetic status reducing the flow to 7.5% of the control flow rate produced a significant ischaemic insult. Separate experiments showed that low-flow ischaemia caused action potential duration (APD) shortening which could be prevented by the KATP channel inhibitor glibenclamide, so implicating the KATP channel in the shortening process. In the second section it was established that low-flow ischaemia caused an early increase in 86Rb efflux which was maximal during the phase of APD shortening. Once again glibenclamide abolished APD shortening but only reduced the degree of 86Rb efflux. In the third section the effects of respiratory and metabolic acidosis, both known modulators of channel function, on the APD were investigated to establish whether they caused KATP channel activation in isolation in whole heart. In conclusion, this study has demonstrated that in whole heart low-flow ischaemia causes potassium efflux as a result of KATP channel activation, with the subsequent APD shortening. Intracellular acidosis and increased intracellular lactate, both known modulators of channel function in isolated patches, cause activation of the channel in isolation in whole heart but their main effect is to cause APD lengthening. Hence, these metabolic changes during ischaemia may serve to reduce overall APD shortening.
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Reaich, David. "Protein and carbohydrate metabolism in metabolic acidosis". Thesis, University of Aberdeen, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308003.

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Chronic renal failure (CRF) is associated with loss of lean body mass, a high incidence of malnutrition, and with insulin resistance. CRF is often complicated by metabolic acidosis. Metabolic acidosis is known to alter both protein and carbohydrate metabolism. A series of studies have been undertaken to investigate the effect of metabolic acidosis on protein metabolism in both normal and CRF human subjects, and to study whether metabolic acidosis in CRF affects insulin sensitivity. Protein turnover was studied using the technique of primed constant infusions of L-[1-13C]leucine. Normal subjects were studied before and after ammonium chloride induced metabolic acidosis. Acidosis was associated with increased protein turnover and amino acid oxidation. In CRF subjects, correction of acidosis with sodium bicarbonate decreased protein turnover and amino acid oxidation. The effect of acidosis in CRF on insulin mediated carbohydrate metabolism was studied using the technique of the hyperinsulinaemic euglycaemic clamp. Insulin sensitivity increased with correction of acidosis. By combining L-[1-13C]leucine infusions with hyperinsulinaemic euglycaemic clamps, the response of protein metabolism to hyperinsulinaemia was measured before and after correction of acidosis. The presence of acidosis did not impair the ability of insulin to modulate protein metabolism. There is therefore, dissociation between the effects of acidosis in CRF on insulin mediated carbohydrate metabolism and insulin mediated protein metabolism. In summary, metabolic acidosis increases protein catabolism in both normal and CRF man and may contribute to the loss of lean body mass characteristic of CRF. Insulin resistance in CRF improves with correction of acidosis. However the effects of acidosis on protein metabolism are not mediated via alterations in insulin sensitivity.
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Herbst, Andreas. "Acidemia at birth risk factors, diagnosis and prognosis, with special reference to maternal fever in labour /". Lund : Dept. of Obstetrics and Gynaecology, University of Lund, 1997. http://books.google.com/books?id=dF9rAAAAMAAJ.

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Li, Ping-An. "Mechanisms of acidosis-mediated ischemic brain damage histopathology and pathophysiology /". Lund : Lund University, 1996. http://catalog.hathitrust.org/api/volumes/oclc/38158955.html.

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Key, M. L. "Acidosis, a fundamental regulator of bone cell function". Thesis, University College London (University of London), 2012. http://discovery.ucl.ac.uk/1361011/.

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Previous work has demonstrated that bone cells are highly sensitive to extracellular acidification. Low pH is a key osteoclast activation factor, and reduces bone formation by inhibiting mineralisation of the matrix. The aim of this thesis was to investigate further the roles played by pH in modulating bone cell function. Transient receptor potential (TRP) channels detect protons within the pathophysiological range, so are potential candidates for mediating the observed effects of acid on bone cells. I found that TRPV1 agonists/antagonists had no effect on osteoclast formation and activation or bone mineralisation by osteoblasts. Additionally, TRPV1-/- osteoclasts demonstrated no functional differences from wildtypes. Furthermore, agonists/antagonists for TRPM8, TRPV4 and TRPV3 were without effect. Pyrophosphate (PPi) a fundamental inhibitor of mineralisation in the bone microenvironment is generated from extracellular nucleotides by ecto-nucleotidases such as E-NPP1. I showed that E-NPP1 mRNA and protein were up-regulated in osteoblasts cultured at pH 6.9; total E-NPP activity was also increased. To determine the role of acidification in tumour-induced osteolysis, I devised an in vitro model to investigate interactions of osteoclasts with breast cancer cells, which metastasise to bone, sometimes causing osteolytic disease. Surprisingly, the overall effect of breast cancer cells on osteoclasts was inhibitory; however, resorption was significantly stimulated relative to buffered controls when breast cancer cells were allowed to acidify the culture medium. These results suggest that local acidification in tumour settings in vivo could be an important factor in determining the degree of osteolysis that occurs. Finally, I investigated whether two key cytokines implicated in the vicious cycle model of tumour-mediated osteolysis, B-cell activating factor (BAFF) and activin A influence osteoclast function. In all experiments only acidosis stimulated osteoclast resorption. These results provide further evidence for the fundamental role of acid as a regulator of bone cell function.
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Książki na temat "Acidosis"

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E. Wesson, Donald, red. Metabolic Acidosis. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3463-8.

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Muñoz, Ricardo, red. Renal Tubular Acidosis in Children. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-91940-5.

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Langbroek, Aart Jan Mattheüs. Metabolic acidosis and ventilatory response. Groningen: Drucker:] van Denderen, 1988.

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Arieff, Allen I., red. Hypoxia, Metabolic Acidosis, and the Circulation. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4614-7542-2.

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1938-, Arieff Allen I., i American Physiological Society (1887- ), red. Hypoxia, metabolic acidosis, and the circulation. New York: Published for the American Physiological Society by Oxford University Press, 1992.

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Parker, James N., i Philip M. Parker. The Official patient's sourcebook on renal tubular acidosis. San Diego, Calif: Icon Health Publications, 2002.

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Rai, Sharadindu. Protective effects of acidosis against stretch-induced lung injury. Ottawa: National Library of Canada, 2002.

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Chŏn, Yang-suk. Chongyang ŭi sansŏnghwa e ŭihan HIF-1[alpha] kwabarhyŏn kijŏn kyumyŏng kwa saeroun hangam chʻiryo tʻaget ŭi palgul =: Mechanism of HIF-1[alpha] overexpression in acidified tumor and novel target for anticancer therapy. [Seoul]: Pogŏn Pokchibu, 2007.

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John, Gennari F., red. Acid-base disorders and their treatment. Boca Raton: Taylor & Francis, 2005.

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Simonsohn, Barbara. Healing power of papaya: A holistic handbook on how to avoid acidosis, allergies, and other health disorders. Twin Lakes, WI: Lotus Light Publications, 2000.

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Części książek na temat "Acidosis"

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Mehlhorn, Heinz. "Acidosis". W Encyclopedia of Parasitology, 57. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_4426.

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Mehlhorn, Heinz. "Acidosis". W Encyclopedia of Parasitology, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_4426-1.

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Böning, Dieter, Michael I. Lindinger, Damian M. Bailey, Istvan Berczi, Kameljit Kalsi, José González-Alonso, David J. Dyck i in. "Acidosis". W Encyclopedia of Exercise Medicine in Health and Disease, 5–7. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_3.

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Goraya, Nimrit, i Donald E. Wesson. "Overview of Acid–Base Physiology". W Metabolic Acidosis, 1–6. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3463-8_1.

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Amodu, Afolarin, i Matthew K. Abramowitz. "Effects of Metabolic Acidosis on Skeletal Muscle". W Metabolic Acidosis, 101–10. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3463-8_10.

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E. Wesson, Donald. "Metabolic Acidosis Effects on Bone and Its Metabolism". W Metabolic Acidosis, 111–20. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3463-8_11.

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E. Wesson, Donald. "Endocrine Consequences of Metabolic Acidosis". W Metabolic Acidosis, 121–30. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3463-8_12.

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Kovesdy, Csaba P. "Metabolic Acidosis and Progression of Chronic Kidney Disease". W Metabolic Acidosis, 131–43. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3463-8_13.

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E. Wesson, Donald. "Management of Chronic Metabolic Acidosis". W Metabolic Acidosis, 145–53. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3463-8_14.

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Laski, Melvin E. "Metabolic Acidosis: Physiology, Presentation, and Diagnosis". W Metabolic Acidosis, 7–16. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3463-8_2.

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Streszczenia konferencji na temat "Acidosis"

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Onanyan, M., I. Garrison, R. White, M. Crook, T. Stevens i J. Y. Lee. "Extrinsic Acidosis Suppresses Lung Endothelium Metabolism While Intrinsic Acidosis Does Not". W American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a1988.

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Nechipurenko, Yury Dmitrievich, Denis Aleksandrovich Semyonov, Igor Andreevich Lavrinenko, Denis Anatolievich Lagutkin, Evgenii Aleksandrovich Generalov, Anna Yurevna Zaitceva, Olga Vyacheslavovna Matveeva i Yegor Evgenievich Yegorov. "PATHOGENESIS OF COVID-19: THE ROLE OF ACIDOSIS". W NEW TECHNOLOGIES IN MEDICINE, BIOLOGY, PHARMACOLOGY AND ECOLOGY. Institute of information technology, 2021. http://dx.doi.org/10.47501/978-5-6044060-1-4.43.

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The article considers a number of positive feedbacks between the damaging factors of COVID-19 and acidosis. The interaction of hypoxia and acidosis is shown. In particular, in accordance with the Bohr effect, a decrease in blood pH leads to a drop in saturation and contributes to the further development of acidosis.
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Raoof, S. "Metformin Associated Lactic Acidosis". W American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4805.

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Tsay, Junchieh J., Derrick Raptis i David R. Schwartz. "Lactic Acidosis In Metastatic Melanoma". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a4609.

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Leiser, A., R. Virdee i P. Kinniry. "Severe Epinephrine-Induced Lactic Acidosis". W American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a3414.

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Ganta, Ashwin, Ratna Priya Gangi, Wilson Gonsalves, Sonica Saini i Tammy Wichman. "Inhalational Beta Agonist Induced Lactic Acidosis". W American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1343.

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Jeyaraman, Alagusutha, Neil Wright i Marta Cohen. "227 Mind the gap!! uncommon cause of high anion gap metabolic acidosis due to pyroglutamic acidosis (PGA)". W RCPCH Conference Singapore. BMJ Publishing Group Ltd, 2021. http://dx.doi.org/10.1136/bmjpo-2021-rcpch.124.

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Gheorghe, MC, R. Dadu, F. Berianu, R. Vazquez, Y. Feng, C. Blot, A. Balasingham, D. Kaufman i CA Manthous. "Hyperchloremic Metabolic Acidosis Following Resuscitation of Shock." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1595.

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Moe, Orson W., Daniel G. Fuster, Xiao-Song Xie, James C. Williams, Andrew P. Evan, James E. Lingeman i James A. McAteer. "Distal Renal Tubular Acidosis and Calcium Nephrolithiasis". W RENAL STONE DISEASE 2: 2nd International Urolithiasis Research Symposium. AIP, 2008. http://dx.doi.org/10.1063/1.2998065.

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El-Kenawi, Asmaa E., Arig A. Ibrahim-Hashim, Kimberly A. Luddy, Shari A. Pilon-Thomas, Robert A. Gatenby i Robert J. Gillies. "Abstract 3213: Extracellular acidosis alters polarization of macrophages". W Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-3213.

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Raporty organizacyjne na temat "Acidosis"

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Rodriquez, Fernando, Mark A. Rasmussen i Milton J. Allison. Discovery of a Probiotic to Reduce the Risk of Lactic Acidosis in Cattle. Ames (Iowa): Iowa State University, styczeń 2007. http://dx.doi.org/10.31274/ans_air-180814-563.

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Chiquette, Johanne, Milton J. Allison i Mark A. Rasmussen. Use of Prevotella bryantii 25A as a Probiotic to Reduce the Risk of Ruminal Acidosis in Dairy Cows. Ames (Iowa): Iowa State University, styczeń 2008. http://dx.doi.org/10.31274/ans_air-180814-161.

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Visser, Wesley, Elma van de Braak, Anneke de Mik - van Egmond, Anna van der Burgh, Nicole de Roos, Inez Jans, Iris van der Hoef, Joanne Olieman, Ewout Hoorn i David Severs. Correcting metabolic acidosis and the nutritional status of patients with non-dialysis dependent chronic kidney disease: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, maj 2023. http://dx.doi.org/10.37766/inplasy2023.5.0085.

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Review question / Objective: What is the effect of correcting metabolic acidosis on different nutritional status parameters in patients with CKD. Information sources: The search was conducted in MEDLINE and the Cochrane Library from inception to December 2022. Two investigators extracted the data independently. Titles and abstracts were screened based on predefined inclusion and exclusion criteria in the protocol. Similarly, full-text articles were screened using a predefined form to extract data. These included year of publication, study design and setting, population characteristics, description of intervention and control conditions, number of patients, and baseline and follow-up outcomes of interest. We requested any relevant missing information from original study authors and received the raw data from one author.
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Guerreiro, Hugo, Rute Borrego i Lino Mendes. β-alanine supplementation for athletic performance in female athletes: a protocol for a systematic review of randomized control trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, czerwiec 2022. http://dx.doi.org/10.37766/inplasy2022.6.0041.

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Review question / Objective: The Effect of β-alanine Supplementation on Athletic Performance in Female Athletes: a Systematic Review of Randomized Control Trials. Condition being studied: β-alanine is an endogenously produced non-proteinogenic amino acid that can also be obtained through the consumption of foods such as meat. The ergogenic effect of β-alanine supplementation is linked to the levels of carnosine (a cytoplasmatic dipeptide to which β-alanine is a precursor). It has become one of the most common sports nutrition ergogenic aids, with typical doses at about 4 to 6 g per day that are ideal to elevate muscle carnosine concentrations by up 80%. This elevation happens regardless of high or low baseline levels (common in vegetarians, women and in older subjects) and chronic supplementation (and the associated increase of muscle carnosine levels) is known to be of particular interest in improving high-intensity exercise performance by enhancing intracellular H+ buffering, reducing muscle acidosis. It has been mostly proposed as beneficial in exercises between 60 seconds and 4 minutes, but some positive effects have been noted in other sport-related outcomes. The fact that women tend to have less muscle carnosine content then man, in addition to other characteristics of the female athlete, highlights the importance of understanding if the outcomes and magnitude of the effects already found and stablished in male athletes are, in fact, equivalent in the female athlete.
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Bannink, A., J. Dijkstra i S. J. Koopmans. Relaties tussen acidose in de pens, in de darm en in het metabolisme van melkvee tijdens de vroege lactatie : deskstudie. Wageningen: Wageningen Livestock Research, 2018. http://dx.doi.org/10.18174/465646.

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