bluuebunny/crossref_metadata_2025_split huggingface dataset:
Neurochemical characterization of pERK-expressing spinal neurons in histamine-induced itch
Authors: Jiang Guan-Yu , Dai Meng-Han , Huang Kun , Chai Guo-Dong , Chen Jia-Yin , Chen Ling , Lang Bing , Wang Qing-Xiu , St Clair David , McCaig Colin , Ding Yu-Qiang , Zhang Ling 
Published: August 2015

AbstractAcute itch is divided into histamine- and non-histamine-dependent subtypes and our previous study has shown that activation of ERK signaling in the spinal dorsal horn (SDH) is required selectively for histamine-induced itch sensation. Morphological characteristics of pERK-expressing neurons are required for exploring the mechanism underlying spinal itch sensation. To investigate whether pERK-expressing neurons are supraspinally-projecting neurons, we injected Fluorogold (FG) into the ventrobasal thalamic complex (VB) and parabrachial region, the two major spinal ascending sites in rodents. A small number (1%) of pERK-positive neurons were labeled by FG, suggesting that histamine-induced activation of ERK is primarily located in local SDH neurons. We then examined the co-localization of pERK with Calbindin and Lmx1b, which are expressed by excitatory neurons and found that more than half (58%) of pERK-positive neurons expressed Lmx1b, but no co-expression with Calbindin was observed. On the other hand, approximately 7% of pERK-positive neurons expressed GAD67 and 27% of them contained Pax2. These results support the idea that pERK-expressing neurons serve as a component of local neuronal circuits for processing itch sensation in the spinal cord.
Detection of attempted movement from the EEG during neuromuscular block: proof of principle study in awake volunteers
Authors: Blokland Yvonne , Spyrou Loukianos , Lerou Jos , Mourisse Jo , Jan Scheffer Gert , Geffen Geert-Jan van , Farquhar Jason , Bruhn Jörgen 
Published: August 2015

AbstractBrain-Computer Interfaces (BCIs) have the potential to detect intraoperative awareness during general anaesthesia. Traditionally, BCI research is aimed at establishing or improving communication and control for patients with permanent paralysis. Patients experiencing intraoperative awareness also lack the means to communicate after administration of a neuromuscular blocker, but may attempt to move. This study evaluates the principle of detecting attempted movements from the electroencephalogram (EEG) during local temporary neuromuscular blockade. EEG was obtained from four healthy volunteers making 3-second hand movements, both before and after local administration of rocuronium in one isolated forearm. Using offline classification analysis we investigated whether the attempted movements the participants made during paralysis could be distinguished from the periods when they did not move or attempt to move. Attempted movement trials were correctly identified in 81 (68–94)% (mean (95% CI)) and 84 (74–93)% of the cases using 30 and 9 EEG channels, respectively. Similar accuracies were obtained when training the classifier on the participants’ actual movements. These results provide proof of the principle that a BCI can detect movement attempts during neuromuscular blockade. Based on this, in the future a BCI may serve as a communication channel between a patient under general anaesthesia and the anaesthesiologist.
Effects of Exendin-4 on bone marrow mesenchymal stem cell proliferation, migration and apoptosis in vitro
Authors: Zhou Hao , Li Dandan , Shi Chen , Xin Ting , Yang Junjie , Zhou Ying , Hu Shunyin , Tian Feng , Wang Jing , Chen Yundai 
Published: August 2015

AbstractMesenchymal stem cells (MSC) are regarded as an attractive source of therapeutic stem cells for myocardial infarction. However, their limited self-renewal capacity, low migration capacity and poor viability after transplantation hamper the clinical use of MSC; thus, a strategy to enhance the biological functions of MSC is required. Exendin-4 (Ex-4), a glucagon-like peptide-1 receptor agonist, exerts cell-protective effects on many types of cells. However, little information is available regarding the influence of Ex-4 on MSC. In our study, MSC were isolated from bone marrow and cultured in vitro. After treatment with Ex-4, MSC displayed a higher proliferative capacity, increased C-X-C motif receptor 4 (CXCR4) expression and an enhanced migration response. Moreover, in H2O2-induced apoptosis, Ex-4 preserved mitochondrial function through scavenging ROS and balancing the expression of anti- and pro-apoptotic proteins, leading to the inhibition of the mitochondria-dependent cell death pathways and increased cell survival. Moreover, higher phospho-Akt (p-Akt) expression was observed after Ex-4 intervention. However, blockade of the PI3K/Akt pathway with inhibitors suppressed the above cytoprotective effects of Ex-4, suggesting that the PI3K/Akt pathway is partly responsible for Ex-4-mediated MSC growth, mobilization and survival. These findings provide an attractive method of maximizing the effectiveness of MSC-based therapies in clinical applications.
Metabolomics analysis reveals the association between lipid abnormalities and oxidative stress, inflammation, fibrosis and Nrf2 dysfunction in aristolochic acid-induced nephropathy
Authors: Zhao Ying-Yong , Wang Hui-Ling , Cheng Xian-Long , Wei Feng , Bai Xu , Lin Rui-Chao , Vaziri Nosratola D. 
Published: August 2015

AbstractAlternative medicines are commonly used for the disease prevention and treatment worldwide. Aristolochic acid (AAI) nephropathy (AAN) is a common and rapidly progressive interstitial nephropathy caused by ingestion of Aristolochia herbal medications. Available data on pathophysiology and molecular mechanisms of AAN are limited and were explored here. SD rats were randomized to AAN and control groups. AAN group was treated with AAI by oral gavage for 12 weeks and observed for additional 12 weeks. Kidneys were processed for histological evaluation, Western blotting and metabolomics analyses using UPLC-QTOF/HDMS. The concentrations of two phosphatidylcholines, two diglycerides and two acyl-carnitines were significantly altered in AAI treated rats at week 4 when renal function and histology were unchanged. Data obtained on weeks 8 to 24 revealed progressive tubulointerstitial fibrosis, inflammation, renal dysfunction, activation of NF-κB, TGF-β and oxidative pathways, impaired Nrf2 system and profound changes in lipid metabolites including numerous PC, lysoPC, PE, lysoPE, ceramides and triglycerides. In conclusion, exposure to AAI results in dynamic changes in kidney tissue fatty acid, phospholipid and glycerolipid metabolisms prior to and after the onset of detectable changes in renal function or histology. These findings point to participation of altered tissue lipid metabolism in the pathogenesis of AAN.
Studies with Angiotensins I and II; The Use of Phenylthiocarbamyl-Derivatives
Authors: Osborn E. C. , Pickens P. T. , Willicombe P. R. , Pirie A. T. , Mahler R. F. 
Published: August 2015

1. Intravenous injections of pure angiotensin I and angiotensin II give similar blood pressure responses in the rat, rabbit and guinea-pig although angiotensin I is generally regarded to be the inactive precursor of angiotensin II.
2. The conversion of angiotensin I to angiotensin II and of phenylthiocarbamyl (PTC)-angiotensin I to PTC-angiotensin II in human blood and plasma was studied using the rat colon as the assay tissue.
3. The results suggest that the rate of conversion of angiotensin I to angiotensin II in blood and plasma is insufficient to explain the comparable activities of angiotensin I and angiotensin II in raising the blood pressure.
Angiotensin Blood Levels during the Evolution of Acute Renal Failure
Authors: Ochoa E. , Finkielman S. , Agrest A. 
Published: August 2015

1. Angiotensin blood levels (ABL) have been measured in thirteen white patients with diagnoses of acute renal failure of different aetiologies during several stages of the disease and with no evidence of other conditions that could stimulate renin release by the kidney.
2. Mean ABL on admission was 770 SEM 62 ng/l. When daily urinary volume was higher than 1500 ml, these values were significantly lower: 114 SEM 49·6 ng/l.
3. A negative correlation between ABL and systolic blood pressure was obtained (r = −0·35, P = 0·01). The partial correlation coefficients between ABL and systolic blood pressure showed the same results.
4. A negative correlation between the logarithm of ABL and daily urinary volume was obtained. The partial linear correlation coefficients between ABL and urine volume confirmed this relationship.
5. There was no correlation between the ABL and the aetiology of the anuria, its final course, the duration of the disease, the arterial blood pressure and the plasma urea, sodium or potassium levels.
6. It is suggested that the decrease in the ABL has some connection with the re-establishment of the diuresis, possibly through an increase of glomerular filtration rate and in sodium excretion affecting the macula densa cells.
Propranolol Block of Adrenaline-Induced Hypophosphataemia in Man
Authors: Massara F. , Camanni F. 
Published: August 2015

1. The effect of propranolol on adrenaline- and insulin-induced hypophosphataemia was studied in man.
2. β-Adrenergic blockade with propranolol almost completely abolished and significantly inhibited adrenaline- and insulin-induced hypophosphataemia respectively; in addition, the drug clearly prevented the normally observed rise in plasma lactate, while causing only a slight change in blood glucose levels.
3. It is suggested that the fall in blood phosphate values induced by adrenaline and, in part, that caused by insulin, is mediated by β-adrenergic receptors.
The Mechanism of Diuresis Caused by Renal Lymphatic Obstruction
Authors: Wada T. , Ogawa M. , Ishikawa J. , Yamauchi M. , Kato E. , Asano S. 
Published: August 2015

1. The effect of renal lymphatic obstruction was studied by clearance methods with special reference to the renal response to the change in extra-cellular fluid (ECF) volume.
2. When the left renal lymphatics of anaesthetized dogs were obstructed, E/C (experimental over control kidney) ratios of urine volume (V) and sodium excretion (UNaV) increased significantly in spite of constancy of GFR E/C. This effect occurred during nondiuresis, water diuresis and during distal blockade (i.e. tubular inhibition by thiazide and ethacrynic acid).
3. As ECF was reduced by distal blockade, V and UNaV decreased rapidly in the control kidney, but only slightly in the experimental one, resulting in a sharp increase of V E/C and UNaV E/C.
4. The results indicate that intrarenal interstitial volume and/or pressure play an important role in sodium and water excretion and that it alters the renal response to a change in ECF volume.
The Urinary Excretion of Lysozyme in Dogs
Authors: Harrison J. F. , Barnes A. D. 
Published: August 2015

1. Twelve dogs under light anaesthesia were infused with creatinine, lysozyme and other proteins, and the femoral arterial and urinary concentrations of the infused substances were measured. In some experiments renal venous blood was withdrawn through a catheter inserted by laparotomy.
2. The glomerular permeability to lysozyme was estimated to be 38% of the permeability to creatinine, but there was wide variation and the standard deviation was 11%.
3. The maximum tubular reabsorptive capacity for lysozyme was estimated to be 1·0 mg/100 ml glomerular filtrate, SD 0·44 mg/100 ml.
4. The renal threshold for lysozyme was about 1·0 mg/100 ml.
5. There was evidence supporting the hypothesis that reabsorbed lysozyme is catabolized and no evidence of reabsorption of intact lysozyme into the blood stream.
6. Infusion of myglobin, Bence Jones protein and ovalbumin had no effect on the excretion of endogenous or exogenous (infused) lysozyme.
7. Lysozyme infusions had no conclusive effect on the excretion of (infused) Bence Jones protein or ovalbumin.
8. Corrections, based on the recovery in vitro of lysozyme activity from dog serum and urine, do not significantly alter the results.
Blood Pressure Lability in Ischaemic Cerebrovascular Disease
Authors: Gross M. , Marshall J. 
Published: August 2015

1. In a survey of blood pressures taken over 24-hr periods by automatic monitoring in a series of men with ischaemic cerebrovascular disease, the variances of the readings were used to compare the lability of blood pressure in subjects subdivided according to the territory of the vascular disorder.
2. The findings that diastolic variance during the daytime in vertebrobasilar ischaemia was significantly higher than in controls and that in both carotid and vertebrobasilar ischaemia, but not controls, daytime variance was higher than night variance, were explicable on the basis that variance is directly related to the height of the blood pressure.
3. There was no evidence that cerebral ischaemia itself, whether in the carotid or vertebrobasilar territories, was associated with abnormal blood pressure lability.
4. It did not appear likely that there was any significant difference between blood pressure lability in subjects who had had cerebral infarction and those who had had transient ischaemic attacks.
Studies by Quantitative Immunoelectrophoresis on Iron Binding Proteins in Haemochromatosis
Authors: Amin A. H. , Clarke H. G. , Freeman T. , Lyon I. M. Murray , Smith P. M. , Williams R. 
Published: August 2015

1. The concentrations of a number of plasma proteins in patients with haemochromatosis were determined by quantitative immunoelectrophoresis, particular attention being paid to the three iron transporting proteins.
2. Transferrin and haptoglobin were within normal limits; haemopexin was significantly greater than normal (P &lt; 0·001).
3. Other changes observed were a significant (P &lt; 0·001) increase of α1 antitrypsin, of α2 macroglobulin and β1A-C; these changes are discussed.
The Early Effects of Dihydrotachysterol on Calcium and Phosphorus Metabolism in Patients with Hypoparathyroidism
Authors: Hunt G. , Morgan D. B. 
Published: August 2015

1. Five patients with chronic hypoparathyroidism were given dihydrotachysterol.
2. Calcium and phosphorus absorption and excretion were measured in three of the patients. An increased absorption of calcium from the intestine was the major source of the increased excretion of calcium after dihydrotachysterol.
3. A change in the renal tubular handling of phosphorus was a major factor in the changes in the serum phosphorus after treatment with dihydrotachysterol.
4. The results suggest that there is a difference between organ responses in any one individual, and that differences in a given organ response between individuals cannot be entirely attributed to the dose of dihydrotachysterol.
5. The implications of these observations for the treatment of hypoparathyroidism are discussed.
The Relation between the Rate of Production of Gastric Juice and its Electrolyte Concentrations
Authors: Hobsley M. , Silen W. 
Published: August 2015

1. Repeated 15-min collections of gastric juice were made during the plateau of response to an intravenous infusion of histamine diphosphate 0·01 mg h−1 kg−1 and the samples measured and their electrolyte concentrations estimated. A linear relationship was found between chloride output and the volume-rate of overall secretion and between hydrogen ion output and the same rate of secretion, while a multivariate linear relationship was also found between all three variables.
2. A mathematical analysis of these results suggests that if gastric secretion consists of an acid and a non-acid component, each of fixed composition, then the acid component has the composition H = 143 mEq/l, K = 16 mEq/l, Cl = 169 mEq/l, and the non-acid component is secreted at the same rate in different subjects under these circumstances.
3. The data enable gross sampling and analytical errors to be detected; in particular, the volume-rate of secretion can be predicted from hydrogen ion concentration, better from chloride ion concentration, and best from the concentrations of both ions.
4. For single samples such predictions appear to be superior to the direct measurement of volume.
The Incorporation of [4-14C] δ-Aminolaevulic Acid into Urinary Porphyrins in Symptomatic Porphyria
Authors: Goldswain P. , Dowdle E. , Spong Norma , Eales L. 
Published: August 2015

1. The specific activities of urinary uroporphyrin and coproporphyrin were measured as functions of time following the administration of a single oral dose of [4-14C] δ-aminolaevulic acid (ALA) to six patients with symptomatic porphyria and one control subject.
2. The peak specific activity of coproporphyrin preceded that of uroporphyrin in all subjects studied and exceeded that of uroporphyrin in the patients with symptomatic porphyria.
3. These results are interpreted as indicating the existence of two distinct metabolic pathways in the liver for the disposal of ALA, rather than as contradicting the generally accepted role of uroporphyrinogen as a precursor of coproporphyrinogen.
Contribution of Hypercapnia and Hypoxia to the Vascular Response to Ischaemia
Authors: Kontos H. A. , Richardson D. W. , Raper A. J. , Patterson J. L. 
Published: August 2015

1. Hypoxia, induced by 7–12% oxygen breathing, produced vasodilatation in the intact or in the phenoxybenzamine and propranolol treated forearm of human volunteers when arterial blood PO2 decreased below 45 mmHg, or when deep forearm venous blood PO2 decreased below 35–40 mmHg.
2. Circulatory arrest of the forearm following alpha and beta adrenergic receptor blockade was followed by greater increases in blood flow and greater decreases in forearm vascular resistance during CO2 breathing than during room air breathing. The increased flow following ischaemia was maintained at a high level until CO2 administration was stopped.
3. The vasodilator response following ischaemia of the human forearm, produced by digital occlusion of the brachial artery, was compared to that produced by hypercapnia or hypoxia or a combination of the two, produced by breathing the appropriate gas mixtures. The forearm was pre-treated with phenoxybenzamine and propranolol to produce alpha and beta adrenergic receptor blockade. For equal increases in deep forearm venous blood PCO2 the vasodilator response to hypercapnia averaged 60% of that following ischaemia. For equal decreases in deep forearm venous blood PO2 the vasodilator response to hypoxia averaged 26% of that produced by ischaemia. The vasodilator response to ischaemia was not modified by breathing 100% oxygen to maintain the deep forearm venous blood PO2 at a level above that seen with the circulation free during room air breathing. Combined hypoxia and hypercapnia of equal severity as those produced by ischaemia resulted in a vasodilator response which averaged 64% of that produced by ischaemia.
The Site of Cardiovascular Action of Angiotensin II in the Brain
Authors: Joy M. D. , Lowe R. D. 
Published: August 2015

1. The site of action of vertebral artery infusions of angiotensin was studied in the chloralose-anaesthetized greyhound.
2. The cardiovascular response to vertebral artery infusion of angiotensin (0·25–2·0 ng kg−1 min−1) was not reduced by clamping the basilar artery between the pons and the pyramidal decussation. There was no response to infusion of angiotensin through a catheter inserted in a rostral direction into the basilar artery above the clamp. The site of action must therefore lie caudal to the pons.
3. Transection of the spinal cord at the first cervical segment did not abolish the response to vertebral artery infusions, which was still mediated by the vagus nerve and abolished by subsequent vagotomy. The site of action must therefore lie rostral to the cervical cord.
4. Local infusions of angiotensin into the small arteries supplying the medulla produced a response similar to that obtained with vertebral artery infusion of angiotensin.
5. These results indicate that the site responsible for these central effects of angiotensin lies in the medulla.
The Effect of Dichlorphenamide on Blood and Cerebrospinal Fluid Acid-Base State in Chronic Ventilatory Failure
Authors: Lane D. J. , Howell J. B. L. , Stretton T. B. 
Published: August 2015

1. Pco2, [HCO−3] and [H+] have been measured in arterial blood and CSF in twenty-three patients with chronic airways obstruction and five patients without chest disease.
2. Through a range of Pco2 in the CSF from normal to 79 mmHg there was a direct linear relation between Pco2 and [H+]. The slope of this relation (0·41 nmol l−1 mmHg−1) was similar to that reported in experimental studies in animals and would appear to represent the extent to which regulatory mechanisms can protect CSF [H+] against the acidosis of chronic hypercapnia.
3. There was also a direct linear relation between CSF [HCO−3] and arterial plasma [HCO−3], the rise in [HCO−3] in the CSF being less than that in the blood.
4. Thirteen patients were re-studied after receiving the carbonic anhydrase inhibitor dichlorphenamide for 1 week. A metabolic acidosis developed in the arterial blood. In the CSF Pco2 and [HCO−3] fell but [H+] did not change. CSF [H+] is maintained constant and normal in other forms of chronic metabolic acidosis but it seems likely that the constancy observed in the present study was fortuitous. Possible reasons for this are discussed, and it is concluded that variability in responsiveness to ventilatory stimuli between patients is the most likely explanation.
Protein Turnover in Skeletal Muscle. II. The Effect of Starvation and a Protein-Free Diet on the Synthesis and Catabolism of Skeletal Muscle Proteins in Comparison to Liver
Authors: Millward D. J. 
Published: August 2015

1. Rates of synthesis and catabolism of liver and muscle sarcoplasmic and myofibrillar protein have been measured in young control, starved and protein (deprived) rats using [14C]Na2CO3 to label protein.
2. Half-lives for synthesis of 1·35, 2·8 and 7·2 days for liver, sarcoplasmic and myofibrillar proteins respectively were obtained, whilst half-lives for catabolism were 1·55, 3·6 and 15·6 days in each case in the control animals.
3. The protein free diet for 3 days caused a small decrease in the rate of synthesis of liver and muscle proteins. The catabolic rate of liver protein was increased by 20% whilst there was a smaller increase in the catabolic rate of myofibrillar proteins.
4. Starvation for 3 days caused a 20% reduction in the rate of liver protein synthesis whilst there were greater reductions in muscle protein synthesis. The catabolic rate of liver protein was only slightly increased whereas there was a 75% increase in the rate of myofibrillar protein breakdown.
5. The total amount of protein synthesis and catabolism in liver and the two muscle protein fractions over the first 3 days of the three regimes were calculated. Muscle protein turnover, in particular myofibrillar, was shown to be very sensitive to dietary protein and/or calorie deficiency.
6. These results are discussed in terms of the mobility and therefore importance of muscle protein metabolism in the economy of the whole animal.