bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interstitial lactate, inosine and hypoxanthine in rat kidney during normothermic ischaemia and recirculation*
Authors: EKLUND T. , WAHLBERG J. , UNGERSTEDT U. , HILLERED L. 
Published: December 2008

The aim of this study was to determine the potential value of extracellular fluid (ECF) lactate, inosine and hypoxanthine for monitoring the disturbance in energy metabolism associated with kidney ischaemia and recirculation, using intrarenal microdialysis as sampling technique. Normothermic ischaemia was produced in rats by clamping of the left renal pedicle. Microdialysis probes were implanted into the renal cortex and the medulla, respectively. Dialysates were collected in 10‐minute fractions before, during 20 (Group A) or 40 minutes (Group B) ischaemia and 2 hours of recirculation. Samples were analysed by HPLC for lactate, inosine and hypoxanthine. Ischaemia caused a dramatic increase of extracellular fluid lactate, inosine and hypoxanthine in both groups, reflecting the disturbance of energy metabolism. The basal extracellular fluid level of lactate as well as that during ischaemia was markedly higher in the medulla compared to cortex, whereas the relative change in lactate concentration was similar (i. e. about 4‐fold). In group A all three metabolites returned to the pre‐ischaemic level within 20 minutes after reperfusion. However, while inosine and hypoxanthine returned promptly to base line in Group B, recovery of lactate varied dramatically between animals suggesting a persistent metabolic disturbance in some rats.Our results indicate that extracellular fluid lactate, inosine and hypoxanthine, measured by intrarenal microdialysis, may be useful for monitoring of the energy state of the kidney during normothermic ischaemia and that extracellular fluid lactate may be a sensitive indicator of post‐ischaemic disturbances in energy metabolism.
Sympathetic nerve stimulation influences mucociliary activity in the rabbit maxillary sinus
Authors: CERVIN A. , LINDBERG S. , MERCKE U. 
Published: December 2008

The effect of preganglionic sympathetic nerve stimulation on mucociliary activity in the rabbit maxillary sinus was investigated in vivo. Response to nerve stimulation was recorded photoelectrically and expressed as a percentage of the basal mucociliary activity prior to stimulation.Nerve stimulation (15 V, 5 ms) for 60 s at 2, 10 and 20 Hz stimulated mucociliary activity, the maximum increase being 21.1 ±1.3% at 20 Hz, an increase that pretreatment with the cholinergic antagonist atropine reduced to 14.5±2.4%, suggesting that part of the response involves cholinergic mechanisms. Nerve stimulation (10 Hz) of animals pretreated with the β‐adrenoceptor antagonist propranolol reversed the mucociliary response from an increase to a decrease (‐10.6± 1.6%), indicating the involvement of β‐receptors in the nerve‐evoked increase. Pretreatment with the α‐adrenoceptor antagonist phentolamine had no effect on response to nerve stimulation. Rabbits given a combined atropine, propranolol and phentolamine blockade manifested decreased mucociliary activity in response to nerve stimulation (‐ 10.6± 2.1 %). Guanethidine pretreatment blocked the effect of nerve stimulation on mucociliary activity, including the observed decrease after combined blockade, indicating the effect to be mediated via sympathetic nerve fibres.The decrease in mucociliary activity in response to nerve stimulation after combined cholinergic‐, β‐, and α‐adrenoceptor blockade suggests the presence of a nonadrenergic, non‐cholinergic inhibitory mechanism. It is possible that this effect is mediated by release of neuropeptide Y, as intraarterial injections of neuropeptide Y reduce mucociliary activity in the rabbit maxillary sinus, and as neuropeptide Y is released in the upper airways upon sympathetic nerve stimulation.
Galanin receptors and their second messengers in the lumbar dorsal spinal cord
Authors: BEDECS K. , LANGEL Ü. , BARTFAI T. , WIESENFELD‐HALLIN Z. 
Published: December 2008

The ligand binding properties of galanin receptors were examined in crude synaptosomal fraction preparations of lumbar dorsal spinal cord, using chloramin‐T mono‐iodinated porcine Tyr26 galanin as ligand.The equilibrium binding of [125I]galanin showed the presence of a single population of high‐affinity binding sites with KD= 0.6±0.2 nM in a concentration of 55±15 fmol mg‐1 protein (Bmax.The N‐terminal fragments galanin (1–16) and galanin (1–12) fully displaced specific [1251]galanin binding from membranes with IC50 values 6 nM and 4 μM, respectively. The C‐terminal fragment galanin (17–29) did not displace [125I]galanin when applied in the concentration range 10‐11–10‐4 M. GTP inhibited the specific binding of [125I] galanin in a concentration dependent manner, with 54% inhibition at 1 mM, suggesting that the galanin receptor found in lumbar dorsal spinal cord is G‐protein coupled.Second messenger systems, through which the galanin receptor in lumbar dorsal spinal cord may exert its effect, were also studied. A galanin (10,μm) produced inhibition (58%) of the depolarization induced cGMP increase was found, whereas galanin (10 μM) did not inhibit the noradrenalin (100 μM) activated CAMP synthesis or phosphoinositide turnover in tissue slices of the spinal cord.Bilateral transection of the sciatic nerve at midthigh level 14 days prior to the binding experiment was performed, a treatment which is known to cause a dramatic increase of galanin‐like immunoreactivity in the superficial layers of the dorsal spinal cord, dorsal root ganglion and in galanin mRNA levels, but no significant effect on Bmax or KD of the galanin receptor was found.
Myosin heavy chain isoform transition in ageing fast and slow muscles of the rat
Authors: SUGIURA T. , MATOBA H. , MIYATA H. , KAWAI Y. , MURAKAMI N. 
Published: December 2008

Sugiura, T., Matoba, H., Miyata, H., Kawai, Y. & Murakami, N. 1992. Myosin heavy chain isoform transition in ageing fast and slow muscles of the rat. Acta Physiol Scand144, 419423. Received 26 August 1991, accepted 3 December 1991. ISSN 0001–6772. Laboratory of Biomechanics and Physiology, Faculty of Liberal Arts, Yamaguchi University, Yamaguchi, Faculty of Integrated Arts and Sciences, Tokushima University, Tokushima, and Department of Physiology, Yamaguchi University School of Medicine, Ube, Yamaguchi, Japan.Using gradient sodium dodecyl sulphate‐polyacrylamide gel electrophoresis, myosin heavy chain (MHC) isoforms were studied in the extensor digitorum longus (EDI,) and the soleus muscles of male Wistar rats at different ages (5, 10, 20 weeks, 1 and 2 years). In the EDL muscle, four types of MHC isoforms were observed in all age groups. There was an increase in the percentage of HCIId and a concomitant decrease in the percentage of HCIIb with increasing age. No significant difference was observed in the percentages of HCI and HCIIa isoforms in all the age groups. In contrast, the soleus muscle contained two MHC isoforms, HCI and HCIIa. There was an increase in the percentage of HCI and a concomitant decrease in the percentage of HCIIa with increasing age. These results suggest that age‐related changes in the MHC isoforms in both the fast‐twitch EDI, and the slow‐twitch soleus muscles are one factor underlying the age‐related decrease in the speed of muscle contraction.
Dopamine and vasoactive intestinal peptide stimulate cyclic adenosine‐3,5 ‐monophosphate formation in isolated rat villus and crypt duodenocytes
Authors: SÄFSTEN B. , FLEMSTRÖM G. 
Published: December 2008

Secretion of bicarbonate increases the pH at the duodenal mucosal surface, a process which contributes to the protection against acid/pepsin injury. Previously, we have shown that dopaminergic compounds stimulate the duodenal bicarbonate secretionin situ, in the anaesthetized rat, through an action on peripheral dopamine D1 receptors. In order to study the possible involvement of cyclic adenosine‐3′,5′‐monophosphate (cAMP) as an intracellular mediator in enterocytes isolated from rat duodenum, cells were collected by a combination of enzyme treatment and calcium chelation. Two major cell fractions, one mainly from villi and the other mainly of crypt origin, were studied. In the villus cell fraction, the activity of alkaline phosphatase was 1.6 ± 0.2μmol mg protein‐1min‐1and that of sucrase 98.8± 16.4 nmol mg protein‐1min‐1. In the crypt fraction, activities were 0.7 ± 0.1 and 28± 10.5, respectively. Effects of dopamine, two selective dopamine receptor agonists and vasoactive intestinal peptide (VIP) on intracellular accumulation of cAMP were examined by radioimmunoassay (RIA).In the crypt cell fraction, VIP (10‐7M) caused an increase in cAMP which was maximal after 5 min (78 ± 28% above control,P <0.01). In the villus cell fraction, maximal responses to VIP (60 ± 24% above control,P <0.05), did not occur until after 60 min of incubation. In contrast, there were no significant differences between villi and crypt enterocytes in respect to effects of dopamine, the dopamine Dl‐receptor agonist SKF‐38393 and the D2‐receptor agonist quinpirole. Dopamine (10‐5M), as well as SKF‐38393 (10‐5M), increased (P <0.05) cAMP accumulation with a maximal response after 5–15 min of incubation. Quinpirole (10‐5M), decreased (P <0.05) cAMP accumulation in both crypt and villi cell fractions.The results suggest that cAMP is involved as a messenger in dopamine D1 receptor‐mediated stimulation of duodenal ulceroprotective alkaline secretion. The time course of cAMP accumulation induced by the potent duodenal secretagogue VIP is different in crypt and villus cells.
The effects of oestrogen and progesterone on insulin sensitivity in female rats
Authors: KUMAGAI S. , HOLMÄNG A. , BJÖRNTORP P. 
Published: December 2008

The effects of 17‐β‐oestradiol (E2) and progesterone (P) on insulin sensitivity were determined in oophorectomized (OVX) rats by the euglycaemic hyperinsulinaemic clamp technique combined with measurements of insulin‐stimulated 2‐deoxy‐D‐glucose (2‐DOG) transport and glycogen synthesis in white and red parts of the gastrocnemius, the extensor digitorum longus and soleus muscles as well as in the liver (only glycogen synthesis). OVX was followed by insulin resistance in the clamp measurements. This was paralleled by a decreased insulin‐stimulated content of 2‐DOG in muscles, an index of glucose transport. Glycogen synthesis in muscle was also decreased, although to less extent. E2, alone or in combination with P, restored this to values of intact controls, while P alone was followed by insulin resistance. Liver glycogen synthesis was also decreased by OVX but this required combination of E2 and P to be fully restored.It was concluded that particularly E2 plays an important role in the maintenance of normal insulin sensitivity while P alone seems to be followed by insulin resistance, both effects apparently mainly by regulation of glucose uptake in muscle. E2± P may be of importance for maintenance of normal glycogen synthesis in the liver.
Altering the blood‐brain barrier in the rat by intracarotid infusion of polycations: a comparison between protamine, poly‐L‐lysine and poly‐L‐arginine
Authors: WESTERGREN I. , B. JOHANSSON B. 
Published: December 2008

To evaluate the role of surface charge for the blood‐brain barrier permeability, the albumin content was determined in the cerebrospinal fluid and in the brain 1 h after intracarotid infusion of protamine sulphate, a natural polycationic protein with a high content of arginine (mol. wt 4000–4400), poly‐L‐arginine (mol. wt 11600) or poly‐L‐lysine (mol. wt 10200).Five milligrams (4 ± 10‐4 mmol) poly‐L‐arginine increased the albumin content in the brain IS times more than S mg (5 ± 10‐4 mmol) poly‐L‐lysine (P < 0.001) and 3.5 times more than 5 mg (1 times 10‐3 mmol) protamine (P < 0.001); the difference between protamine and poly‐L‐lysine was also significant (P < 0.05). After 0.5 mg (4 ± 10‐4 mmol) poly‐L‐arginine the albumin extravasation was still higher than after 5 mg protamine (P < 0.01) and 5 mg poly‐L‐lysine (P < 0.001). Cisternal albumin increased from control values 0.08 mg ml‐1 to 0.30, 0.46 and 1.21 mg ml‐1 in rats given 5 mg poly‐L‐lysine, protamine and poly‐L‐arginine, respectively (P < 0.01 for difference between arginine and the other two substances).The higher mol. wt and positive charge of poly‐L‐arginine may at least in part explain the more pronounced albumin leakage after arginine than after protamine. However, the difference between poly‐L‐arginine and poly‐L‐lysine suggests that other factors, possibly related to the guanidino groups, contribute to the blood‐brain barrier opening by poly‐L‐arginine.
The antinociceptive effect of non‐noxious sensory stimulation is mediated partly through oxytocinergic mechanisms
Authors: UVNäS‐MOBERG K. , BRUZELIUS G. , ALSTER P. , LUNDEBERG T. 
Published: December 2008

The objective of the present study was to investigate whether oxytocinergic mechanisms may contribute to the antinociceptive effect of non‐noxious, sensory stimulation.To test this hypothesis, oxytocin levels in plasma and cerebrospinal fluid (CSF) were measured in control rats as well as in rats exposed for 30 min to electro‐acupuncture (2 Hz), thermal stimulation (40 oC) or vibration (100 Hz). All modes of stimulation induced significant elevations of oxytocin levels in plasma and/or in CSF, 30 or 90 min after the end of stimulation. Secondly, the antinociceptive effects of these treatments were investigated in the tail‐flick test with and without prior administration of the oxytocin antagonist l‐deamino‐2‐D‐Tyr‐(OEt)‐4‐Thr‐8‐Orn‐oxytocin (1 mg kg‐1 i.p.). All three modes of stimulation caused a significant delay of the tail‐flick latency to the same degree as that caused by injection of oxytocin 1 mg kg‐1 i.p. (electro‐acupuncture P < 0.01, thermal stimulation and vibration P < 0.05). In all cases, the delay was reversed by administration of the oxytocin antagonist (1 rngkg‐1 i.p.). These findings suggest that analgesic effects induced by non‐noxious sensory stimulation may, in part, be mediated through activation of oxytocinergic mechanisms.
Dynamic changes of myocardial inositoltrisphosphate and cyclic nucleotides: relationship to contractile response in the perfused working rat heart after adrenergic and muscarinic agonist stimulation
Authors: MARTINUSSEN H. J. , WALDENSTRÖM A. , RONQJJIST G. 
Published: December 2008

Initial and late effects by adrenergic and muscarinic agonists on inositol (1,4,5) trisphosphate (IP3) and cyclic nucleotide levels were determined and correlated to mechanical response in perfused rat hearts. Forty‐three rat hearts were perfused with Krebs‐Henseleit buffer in a modified Langendorff apparatus as a working preparation. The hearts were perfused as controls (n= 11), or with noradrenaline (10‐6mol 1‐1) (n= 21), or with carbachol (3 × 10‐7mol 1‐1) (n= 11) added to the perfusion buffer. The hearts were frozen at 20 s, 30 s and 40 min after addition of noradrenaline and at 20 s and 40 min after addition of carbachol, and after 5 and 45 min of control perfusion. cAMP and cGMP were determined by radioligand methods and IP3by a combined fast performance liquid chromatography (FPLC) ‐ isotachophoretic method. cAMP increased by 36% within 20 s followed by a decrease (22%) during the 10 s following noradrenaline addition. After 40 min cAMP regained its value near that of 20 s. Noradrenaline perfusion did not influence IP3levels during the first 30 s although the value at 40 min was significantly higher (59%). IP3increased (42%) after 20 s of carbachol perfusion followed by a 25 % decrease at 40 min.Sustained stimulation of β‐receptors (after 40 min in our model) resulted in a repeated increase in cAMP only, without an increase in contractility. Muscarinic receptor stimulation resulted in an early increase in IP3content without a change in mechanical function whereas a‐adrenergic stimulation resulted in only a late increase in IP3content of isolated whole hearts still without any alteration in contractility.
Effect of DNase and Antibiotics on Biofilm Characteristics
Authors: Tetz George V. , Artemenko Natalia K. , Tetz Victor V. 
Published: December 2008

ABSTRACT
The role of extracellular DNA in the maintenance of biofilms formed by gram-positive and gram-negative bacteria was studied. This study evaluated all the bacterial strains that were tested for the presence of extracellular DNA with an average size of 30 kb in the matrix. Our results indicate changes in community biomass, architecture, morphology, and the numbers of CFU in the presence of DNase. This effect seems to be common to biofilms established by various unrelated gram-positive and gram-negative bacteria. The cleavage of extracellular DNA leads to the formation of an altered biofilm that permits the increased penetration of antibiotics. Thus, the addition of DNase enhances the effect of antibiotics, resulting in decreased biofilm biomass and numbers of CFU.
Efficacy of the Novel Diamidine Compound 2,5-Bis(4-Amidinophenyl)- Furan-Bis-
O
-Methlylamidoxime (Pafuramidine, DB289) against
Trypanosoma brucei rhodesiense
Infection in Vervet Monkeys after Oral Administration
Authors: Mdachi R. E. , Thuita J. K. , Kagira J. M. , Ngotho J. M. , Murilla G. A. , Ndung'u J. M. , Tidwell R. R. , Hall J. E. , Brun R. 
Published: December 2008

ABSTRACT

Owing to the lack of oral drugs for human African trypanosomiasis, patients have to be hospitalized for 10 to 30 days to facilitate treatment with parenterally administered medicines. The efficacy of a novel orally administered prodrug, 2,5-bis(4-amidinophenyl)-furan-bis-
O
-methlylamidoxime (pafuramidine, DB289), was tested in the vervet monkey (
Chlorocebus
[
Cercopithecus
]
aethiops
) model of sleeping sickness. Five groups of three animals each were infected intravenously with 10
4
Trypanosoma brucei rhodesiense
KETRI 2537 cells. On the seventh day postinfection (p.i.) in an early-stage infection, animals in groups 1, 2, and 3 were treated orally with pafuramidine at dose rates of 1, 3, or 10 mg/kg of body weight, respectively, for five consecutive days. The animals in groups 4 and 5 were treated with 10 mg/kg for 10 consecutive days starting on the 14th day p.i. (group 4) or on the 28th day p.i. (group 5), when these animals were in the late stage of the disease. In the groups treated in the early stage, 10 mg/kg of pafuramidine completely cured all three monkeys, whereas lower doses of 3 mg/kg and 1 mg/kg cured only one of three and zero of three monkeys, respectively. Treatment of late-stage infections resulted in cure rates of one of three (group 4) and zero of three (group 5) monkeys. These studies demonstrated that pafuramidine was orally active in monkeys with early-stage
T. brucei rhodesiense
infections at dose rates above 3 mg/kg for 5 days. It was also evident that the drug attained only minimal efficacy against late-stage infections, indicating the limited ability of the molecule to cross the blood-brain barrier. This study has shown that oral diamidines have potential for the treatment of early-stage sleeping sickness.
Postantibiotic Effect of Tigecycline against 14 Gram-Positive Organisms
Authors: Pankuch G. A. , Appelbaum P. C. 
Published: December 2008

ABSTRACT

The in vitro postantibiotic effects (PAEs), postantibiotic sub-MIC effects (PA-SMEs), and sub-MIC effects of tigecycline were determined for 14 gram-positive and gram-negative organisms. The pneumococcal, staphylococcal, and enterococcal PAEs were 1.9 to 5.1, 2.9 to 5.7, and 3.9 to 6.1 h, respectively, and those for
Haemophilus influenzae
,
Escherichia coli
,
Klebsiella pneumoniae
,
Enterobacter cloacae
, and
Acinetobacter baumannii
were 1.1 to 5.0, 1.9 to 2.1, 1.7 to 1.8, 1.0 to 1.7, and 0.7 to 3 h, respectively. The PA-SMEs (four times the MIC) ranged from 6.7 to >11 h for gram-positive organisms and from 2.3 to >11.3 h for gram-negative organisms.
Regulatory T Cells Modulate Staphylococcal Enterotoxin B-Induced Effector T-Cell Activation and Acceleration of Colitis
Authors: Heriazon Armando , Zhou Pengfei , Borojevic Rajka , Foerster Katharina , Streutker Catherine J. , Ng Terry , Croitoru Kenneth 
Published: December 2008

ABSTRACTOral administration of bacterial superantigenStaphylococcus aureusenterotoxin B (SEB) activates mucosal T cells but does not cause mucosal inflammation. We examined the effect of oral SEB on the development of mucosal inflammation in mice in the absence of regulatory T (Treg) cells. SCID mice were fed SEB 3 and 7 days after reconstitution with CD4+CD45RBhighor CD4+CD45RBhighplus CD4+CD45RBlowT cells. Mice were sacrificed at different time points to examine changes in tissue damage and in T-cell phenotypes. Feeding SEB failed to produce any clinical effect on SCID mice reconstituted with CD4+CD45RBhighand CD4+CD45RBlowT cells, but feeding SEB accelerated the development of colitis in SCID mice reconstituted with CD4+CD45RBhighT cells alone. The latter was associated with an increase in the number of CD4+Vβ8+T cells expressing CD69 and a significantly lower number of CD4+CD25+Foxp3+T cells. These changes were not observed in SCID mice reconstituted with both CD45RBhighand CD45RBlowT cells. In addition, SEB impaired the development of Treg cells in the SCID mice reconstituted with CD4+CD45RBhighT cells alone but had no direct effect on Treg cells. In the absence of Treg cells, feeding SEB induced activation of mucosal T cells and accelerated the development of colitis. This suggests that Treg cells prevent SEB-induced mucosal inflammation through modulation of SEB-induced T-cell activation.
Human Microbiota-Secreted Factors Inhibit Shiga Toxin Synthesis by Enterohemorrhagic
Escherichia coli
O157:H7
Authors: de Sablet Thibaut , Chassard Christophe , Bernalier-Donadille Annick , Vareille Marjolaine , Gobert Alain P. , Martin Christine 
Published: December 2008

ABSTRACT

Escherichia coli
O157:H7 is a food-borne pathogen causing hemorrhagic colitis and hemolytic-uremic syndrome, especially in children. The main virulence factor responsible for the more serious disease is the Shiga toxin 2 (Stx2), which is released in the gut after oral ingestion of the organism. Although it is accepted that the amount of Stx2 produced by
E. coli
O157:H7 in the gut is critical for the development of disease, the eukaryotic or prokaryotic gut factors that modulate Stx2 synthesis are largely unknown. In this study, we examined the influence of prokaryotic molecules released by a complex human microbiota on Stx2 synthesis by
E. coli
O157:H7. Stx2 synthesis was assessed after growth of
E. coli
O157:H7 in cecal contents of gnotobiotic rats colonized with human microbiota or in conditioned medium having supported the growth of complex human microbiota. Extracellular prokaryotic molecules produced by the commensal microbiota repress
stx
2
mRNA expression and Stx2 production by inhibiting the spontaneous and induced lytic cycle mediated by RecA. These molecules, with a molecular mass of below 3 kDa, are produced in part by
Bacteroides thetaiotaomicron
, a predominant species of the normal human intestinal microbiota. The microbiota-induced
stx
2
repression is independent of the known quorum-sensing pathways described in
E. coli
O157:H7 involving SdiA, QseA, QseC, or autoinducer 3. Our findings demonstrate for the first time the regulatory activity of a soluble factor produced by the complex human digestive microbiota on a bacterial virulence factor in a physiologically relevant context.