bluuebunny/crossref_metadata_2025_split huggingface dataset:
Alpha-2 adrenergic-induced changes in rectal temperature in adult and 13-day old rats following acute and repeated desipramine administration
Authors: Deupree Jean D , Burke William J , Bylund David B 
Published: October 2008

AbstractBackgroundThe effects of acute and repeated treatment with desipramine on the functional response of α2-adrenoceptors were tested in adult and 13-day old rats. The functional response measured was hypothermia that was induced by brimonidine, an α2-adrenoceptor agonist. The change in the extent of the brimonidine-induced hypothermia following pretreatment with either single or 4 twice-daily injections of desipramine was compared in 13-day old and adult (65–75 days old) male rats.ResultsBrimonidine, alone, lowered rectal temperature to a greater extent in juvenile than in adult rats, and this response was dose-dependently blocked by the selective α2-adrenoceptor antagonist, RX821002, in both groups of rats. Single desipramine administration lowered rectal temperature in the absence of brimonidine in adult but not in juvenile rats. The adult rats developed tolerance to this hypothermic effect after 4 days of desipramine treatment (10 mg/kg twice daily). Repeated desipramine treatment of adult rats also resulted in an enhancement in the brimonidine-induced hypothermic effect 24 h after the last dose, a time when above 90% of desipramine and its metabolite, desmethyldesipramine, had cleared the brain, but not at 14, 48 or 96 h after the last dose. In juvenile rats repeated injections of desipramine (3 mg/kg twice daily for 4 days) had no effect on the α2-agonist-induced hypothermia when brimonidine was given 14, 24, 63 and 96 h after the last dose of desipramine.ConclusionThe results suggest that juvenile rats response differently than adult rats to agonist stimulation of α2-adrenoceptors with and without pretreatment with the antidepressant desipramine. In the absence of desipramine pretreatment, the α2-adrenoceptor-induced hypothermic effect in juvenile rats is greater than in adult rats. Acute injections of desipramine, in the absence of agonist produced a hypothermic effect in adult but not juvenile rats. In addition, the increased α2-agonist-induced hypothermic effect following repeated injections of desipramine that is seen in adult rats is not seen in juvenile rats.
Functional analysis of the novel TBX5c.1333delC mutation resulting in an extended TBX5 protein
Authors: Böhm Johann , Heinritz Wolfram , Craig Alexander , Vujic Mihailo , Ekman-Joelsson Britt-Marie , Kohlhase Jürgen , Froster Ursula 
Published: October 2008

Abstract

Background
Autosomal dominant Holt-Oram syndrome (HOS) is caused by mutations in the TBX5 gene and is characterized by congenital heart and preaxial radial ray upper limb defects. Most of the TBX5 mutations found in patients with HOS cause premature truncation of the primary TBX5 transcript. TBX5 missense mutations alter the three-dimensional structure of the protein and result in failed nuclear localization or reduced binding to target DNA. In this study we present our functional analyses of the novel and unusual c.1333delC mutation found in a patient with classical HOS.

Methods
The functional impact of this novel mutation was assessed by investigating the intracellular localization of the resulting TBX5 protein and its ability to activate the expression of its downstream target ANF.

Results
The deletion of the cytosine is the first TBX5 frameshift mutation predicted to result in an elongated TBX5 protein with 74 miscoding amino acids and 62 supernumerary C-terminal amino acids. The c.1333delC mutation affects neither the nuclear localization, nor its colocalization with SALL4, but severely affects the activation of the ANF promoter.

Conclusion
The mutation c.1333delC does not locate within functional domains, but impairs the activation of the downstream target. This suggests that misfolding of the protein prevents its biological function.
The effects of the Mulligan Sustained Natural Apophyseal Glide (SNAG) mobilisation in the lumbar flexion range of asymptomatic subjects as measured by the Zebris CMS20 3-D motion analysis system
Authors: Moutzouri Maria , Billis Evdokia , Strimpakos Nikolaos , Kottika Polixeni , Oldham Jacqueline A 
Published: October 2008

AbstractBackgroundMulligan's mobilisation techniques are thought to increase the range of movement (ROM) in patients with low back pain. The primary aim of this study was to investigate the application of the Mulligan's Sustained Natural Apophyseal Glide (SNAG) technique on lumbar flexion ROM. The secondary aim was to measure the intra- and inter-day reliability of lumbar ROM employing the same procedure.Methods49 asymptomatic volunteers participated in this double-blinded study. Subjects were randomly assigned to receive either SNAG mobilisation (n = 25), or a sham mobilisation (n = 24). The SNAG technique was applied at the L3and L4spinal levels with active flexion in sitting by an experienced manual therapist. Three sets of 10 repetitions at each of the two spinal levels were performed. The sham mobilisation was similar to the SNAG but did not apply the appropriate direction or force. Lumbar ROM was measured by a three dimensional electronic goniometer (Zebris CMS20), before and after each technique. For the reliability, five measurements in two different days (one week apart) were performed in 20 healthy subjects.ResultsWhen both interventions were compared, independentttests yielded no statistically significant results in ROM between groups (p = 0.673). Furthermore no significant within group differences were observed: SNAG (p = 0.842), sham (p = 0.169). Intra- and inter-day reliability of flexion measurements was high (ICC1,1> 0.82, SEM < 4.0°, SDD<16.3%) indicating acceptable clinical applicability.ConclusionWhile the Zebris proved to be a reliable device for measuring lumbar flexion ROM, SNAG mobilisation did not demonstrate significant differences in flexion ROM when compared to sham mobilisation.Trial registrationCurrent Controlled Trials NCT00678093.
One-step refolding and purification of disulfide-containing proteins with a C-terminal MESNA thioester
Authors: Bastings Maartje MC , van Baal Ingrid , Meijer EW , Merkx Maarten 
Published: October 2008

Abstract

Background
Expression systems based on self-cleavable intein domains allow the generation of recombinant proteins with a C-terminal thioester. This uniquely reactive C-terminus can be used in native chemical ligation reactions to introduce synthetic groups or to immobilize proteins on surfaces and nanoparticles. Unfortunately, common refolding procedures for recombinant proteins that contain disulfide bonds do not preserve the thioester functionality and therefore novel refolding procedures need to be developed.

Results
A novel redox buffer consisting of MESNA and diMESNA showed a refolding efficiency comparable to that of GSH/GSSG and prevented loss of the protein's thioester functionality. Moreover, introduction of the MESNA/diMESNA redox couple in the cleavage buffer allowed simultaneous on-column refolding of Ribonuclease A and intein-mediated cleavage to yield Ribonuclease A with a C-terminal MESNA-thioester. The C-terminal thioester was shown to be active in native chemical ligation.

Conclusion
An efficient method was developed for the production of disulfide bond containing proteins with C-terminal thioesters. Introduction of a MESNA/diMESNA redox couple resulted in simultaneous on-column refolding, purification and thioester generation of the model protein Ribonuclease A.
Exercise training in the aerobic/anaerobic metabolic transition prevents glucose intolerance in alloxan-treated rats
Authors: Soares de Alencar Mota Clécia , Ribeiro Carla , de Araújo Gustavo Gomes , de Araújo Michel Barbosa , de Barros Manchado-Gobatto Fúlvia , Voltarelli Fabrício Azevedo , de Oliveira Camila Aparecida Machado , Luciano Eliete , de Mello Maria Alice Rostom 
Published: October 2008

Abstract

Background
Ninety percent of cases of diabetes are of the slowly evolving non-insulin-dependent type, or Type 2 diabetes. Lack of exercise is regarded as one of the main causes of this disorder. In this study we analyzed the effects of physical exercise on glucose homeostasis in adult rats with type 2 diabetes induced by a neonatal injection of alloxan.

Methods
Female Wistar rats aged 6 days were injected with either 250 mg/kg of body weight of alloxan or citrate buffer 0.01 M (controls). After weaning, half of the animals in each group were subjected to physical training adjusted to meet the aerobic-anaerobic metabolic transition by swimming 1 h/day for 5 days a week with weight overloads. The necessary overload used was set and periodically readjusted for each rat through effort tests based on the maximal lactate steady state procedure. When aged 28, 60, 90, and 120 days, the rats underwent glucose tolerance tests (GTT) and their peripheral insulin sensitivity was evaluated using the HOMA index.

Results
The area under the serum glucose curve obtained through GTT was always higher in alloxan-treated animals than in controls. A decrease in this area was observed in trained alloxan-treated rats at 90 and 120 days old compared with non-trained animals. At 90 days old the trained controls showed lower HOMA indices than the non-trained controls.

Conclusion
Neonatal administration of alloxan induced a persistent glucose intolerance in all injected rats, which was successfully counteracted by physical training in the aerobic/anaerobic metabolic transition.
'Rapunzel syndrome' trichobezoar in a 7-year-old girl: a case report
Authors: Al Wadan Ali H , Al Kaff Hamed , Al Senabani Jamila , Al Saadi Azan S 
Published: October 2008

Abstract

Background
Rapunzel syndrome is a rare type of trichobezoar with an extension of the hair into the small bowel. Clinical presentation is deceptive and vague ranging from abdominal mass to gastrointestinal symptoms.

Case presentation
We present a 7 years old girl with Rapunzel syndrome, where the trichobezoar was not suspected at all especially with negative history of trichophagia. In majority of the cases the diagnosis was made very late in the history of the disease, at a stage where surgery is the only cure for this syndrome.

Conclusion
In the paediatric age group with a long history of gastrointestinal symptom, endoscopy is a diagnostic as well as a therapeutic modality and may reduce surgery in trichobezoars.
Basigin-Mediated Gene Expression Changes in Mouse Uterine Stromal Cells During Implantation
Authors: Chen Li , Belton Robert J. , Nowak Romana A. 
Published: October 2008

Implantation of mouse embryos is dependent on the proliferation and differentiation of uterine stromal cells in a process called decidualization. Decidualization both supports and limits the invasion of the implanting embryo and is regulated in part by the expression of matrix metalloproteinases (MMPs) and their inhibitors, the tissue inhibitors of metalloproteinases (TIMPs). Molecules that alter the balance between MMP and TIMP expression could prevent implantation of the embryo. The membrane glycoprotein basigin (CD147/EMMPRIN), a known inducer of MMPs, is necessary for normal implantation in the mouse. The purpose of this study was to investigate the potential roles of basigin during implantation in the mouse. Using an in vitro stromal cell culture system, we found that recombinant human basigin protein (rBSG) increases MMP-3 and MMP-9 expression without altering TIMP-3 expression. Our results also showed rBSG induces expression of cytokines IL-1α/β and leukocyte chemoattractants, CCL3, CCL20, CXCL2, and CXCL5. More importantly, rBSG significantly suppressed stromal cell decidualization as shown by the inhibition of alkaline phosphatase-2 expression and activity by rBSG. However, rBSG did not affect stromal cell proliferation. Taken together, our data indicate that basigin mediates gene expression changes in mouse uterine stromal cells and suggests that temporal and spatial regulation of basigin expression may be involved in the recruitment of leukocytes to the mouse uterus during early pregnancy.The role of basigin during embryo implantation in mice is examined. Basigin regulates matrix metalloproteinase, IL-1, and leukocyte chemoattractant production by uterine stromal cells.
17β-Estradiol Modulates Expression of Low-Voltage-Activated CaV3.2 T-Type Calcium Channel via Extracellularly Regulated Kinase Pathway in Cardiomyocytes
Authors: Marni Farzana , Wang Yan , Morishima Masaki , Shimaoka Toru , Uchino Tomoko , Zheng Mingqi , Kaku Toshihiko , Ono Katsushige 
Published: October 2008

T-type Ca2+ channel current (ICa,T) plays an important role for spontaneous pacemaker activity and is involved in the progression of structural heart diseases. Estrogens are of importance for the regulation of growth and differentiation and function in a wide array of target tissues, including those in the cardiovascular system. The aim of this study was to elucidate the short-term and long-term effects of 17β-estradiol (E2) on ICa,T in cardiomyocytes. We employed in vivo and in vitro techniques to clarify E2-mediated modulation of heart rate (HR) in ovariectomized rats and ICa,T in cardiomyocytes. Ovariectomy increased HR and E2 supplement reduced HR in ovariectomized rats. Slowing of E2-induced HR was consistent with the deceleration of automaticity in E2-treated neonatal cardiomyocytes. Short-term application of E2 did not have significant effects on ICa,T, whereas in cardiomyocytes treated with 10 nm E2 for 24 h, estrogen receptor-independent down-regulation of peak ICa,T and declination of CaV3.2 mRNA were observed. Expression of a cardiac-specific transcription factor Csx/Nkx2.5 was also suppressed by E2 treatment for 24 h. On the other hand, expression of CaV3.1 mRNA was unaltered by E2 treatment in this study. An ERK-1/2, 5 inhibitor, PD-98059, abolished the effects of E2 on ICa,T and CaV3.2 mRNA as well as Csx/Nkx2.5 mRNA. These findings indicate that E2 decreases CaV3.2 ICa,T through activation of ERK-1/2, 5, which is mediated by the suppression of Csx/Nkx2.5-dependent transcription, suggesting a genomic effect of E2 as a negative chronotropic factor in the heart.
Long-term treatment of cardiomyocytes with 17β-estradiol decreases the T-type Ca2+ channel current of CaV3.2 through activation of ERK-1/2, 5, which is mediated by the suppression of a transcription factor Csx/Nkx2.5.
Parathyroid Hormone Contributes to Regulating Milk Calcium Content and Modulates Neonatal Bone Formation Cooperatively with Calcium
Authors: Cao Guofan , Gu Zhen , Ren Yongxin , Shu Lei , Tao Chunxiang , Karaplis Andrew , Goltzman David , Miao Dengshun 
Published: October 2008

To determine whether PTH and calcium (Ca) interact in neonatal bone formation, female lactating mice either heterozygous (PTH+/−) or homozygous (PTH−/−) for targeted deletion of the pth gene were fed either a normal (1% Ca, 0.6% phosphate) or high-Ca diet (2% Ca and 0.4% phosphate). Dietary effects on milk Ca content and Ca-regulating hormones were determined in dams, and the effects of milk content were assessed on bone turnover in 3-wk-old pups. On the normal diet, milk Ca and 1,25-dihydroxyvitamin D3 levels were lower, but milk PTH-related protein levels were higher in the PTH−/− dams compared with the PTH+/− dams. On the high-Ca diet, milk Ca levels were higher, but milk 1,25-dihydroxyvitamin D3 and PTH-related protein levels were lower in both PTH+/− and PTH−/− dams. In pups fed by PTH−/− dams compared with pups fed by PTH+/− dams on normal diets, bone mineral density, trabecular bone volume relative to tissue volume, and the number of osteoblasts were reduced in both PTH+/− (32.5 ± 1.2 vs. 39.6 ± 1.5 mg/cm2, P &lt; 0.05; 23.3 ± 1.6 vs. 29.2 ± 2.8%, P &lt; 0.01; and 94.2 ± 8.2 vs. 123.5 ± 3.5/mm2, P &lt; 0.01, respectively) and PTH−/− (20.4 ± 0.9 vs. 27.0 ± 1.2 mg/mm2, P &lt; 0.05; 16.8 ± 1.9 vs. 19.3 ± 2.1%, P &lt; 0.05; and 48.6 ± 7.9 vs. 90.5 ± 8.6/mm2, P &lt; 0.01, respectively) pups but were lower in the PTH−/− pups compared with the PTH+/− pups. In contrast, in pups fed by either PTH+/− or PTH−/− dams on the high-Ca diet, bone mineral density, bone volume/tissue volume, and osteoblast numbers were significantly higher, in both PTH+/− (50.5 ± 1.7 vs. 58.7 ± 2.0 mg/mm2, P &lt; 0.05; 37.9 ± 5.2 vs. 46.1 ± 5.1, P &lt; 0.05; and 120.5 ± 9.2 vs. 159.3 ± 14.7/mm2, P &lt; 0.01, respectively) and PTH−/− (33.0 ± 1.2 vs. 47.5 ± 2.2 mg/mm2, P &lt; 0.001; 23.8 ± 3.1 vs. 35.9 ± 2.0, P &lt; 0.05; and 78.7 ± 10.1 vs. 99.8 ± 13.6/mm2, P &lt; 0.05, respectively), and were highest in the PTH+/− pups fed by the PTH+/− dams on the high-Ca diet. These results indicate that PTH can modulate Ca content of milk, and that PTH and Ca can each exert cooperative roles on osteoblastic bone formation in the neonate.
PTH can modulate calcium content of maternal milk, and PTH and calcium exert cooperative roles on osteoblastic bone formation in the neonate.
Oxytocin Receptor Down-Regulation Is Not Necessary for Reducing Oxytocin-Induced Prostaglandin F2α Accumulation by Interferon-τ in a Bovine Endometrial Epithelial Cell Line
Authors: Krishnaswamy Narayanan , Danyod Ghislain , Chapdelaine Pierre , Fortier Michel A. 
Published: October 2008

Interferon-τ (IFNτ) is the embryonic signal responsible for pregnancy recognition in ruminants. The primary action of IFNτ is believed to be mediated through inhibition of prostaglandin F2α (PGF2α) released from the endometrial epithelial cells in response to oxytocin (OT). Our working hypothesis was that the antiluteolytic effect of IFNτ also involved modulation of PG production downstream of OT receptor (OTR) and/or cyclooxygenase 2 (COX2). There is currently no OT-sensitive endometrial cell line to study the molecular mechanisms underlying our hypotheses. Therefore, we established an immortalized bovine endometrial epithelial cell line (bEEL) exhibiting OT response. These cells were cytokeratin positive, expressed steroid receptors, and exhibited preferential accumulation of PGF2α over PGE2. The bEEL cells were highly sensitive to OT, showing time- and concentration-dependent increase in COX2 transcript and protein and PGF2α accumulation. Interestingly, IFNτ (20 ng/ml) significantly reduced OT-induced PGF2α accumulation, but surprisingly, the effect was not mediated through down-regulation of either OTR or COX2. Rather, IFNτ up-regulated COX2 in a time- and concentration-dependent manner while decreasing OT-induced PG accumulation. This suggests that COX2 is not a primary target for the antiluteolytic effect of IFNτ. Because IFNτ reduced OT-stimulated PGF2α accumulation within 3 h, the mechanism likely involves a direct interference at the level of the OT signaling or transcription in addition to the down-regulation of OTR observed in vivo. In summary, bEEL cells offer a unique in vitro model for investigating the cellular and molecular mechanisms underlying OT and IFNτ response in relation with luteolysis and recognition of pregnancy in the bovine.
Interferon-τ acts as a competitive partial agonist, stimulating basal but inhibiting oxytocin- and phorbol myristate acetate-stimulated prostaglandin F2α production in immortalized bovine endometrial epithelial cells.
Psychosocial Stress Inhibits Amplitude of Gonadotropin-Releasing Hormone Pulses Independent of Cortisol Action on the Type II Glucocorticoid Receptor
Authors: Wagenmaker Elizabeth R. , Breen Kellie M. , Oakley Amy E. , Tilbrook Alan J. , Karsch Fred J. 
Published: October 2008

Our laboratory has developed a paradigm of psychosocial stress (sequential layering of isolation, blindfold, and predator cues) that robustly elevates cortisol secretion and decreases LH pulse amplitude in ovariectomized ewes. This decrease in LH pulse amplitude is due, at least in part, to a reduction in pituitary responsiveness to GnRH, caused by cortisol acting via the type II glucocorticoid receptor (GR). The first experiment of the current study aimed to determine whether this layered psychosocial stress also inhibits pulsatile GnRH release into pituitary portal blood. The stress paradigm significantly reduced GnRH pulse amplitude compared with nonstressed ovariectomized ewes. The second experiment tested if this stress-induced decrease in GnRH pulse amplitude is mediated by cortisol action on the type II GR. Ovariectomized ewes were allocated to three groups: nonstress control, stress, and stress plus the type II GR antagonist RU486. The layered psychosocial stress paradigm decreased GnRH and LH pulse amplitude compared with nonstress controls. Importantly, the stress also lowered GnRH pulse amplitude to a comparable extent in ewes in which cortisol action via the type II GR was antagonized. Therefore, we conclude that psychosocial stress reduces the amplitude of GnRH pulses independent of cortisol action on the type II GR. The present findings, combined with our recent observations, suggest that the mechanisms by which psychosocial stress inhibits reproductive neuroendocrine activity at the hypothalamic and pituitary levels are fundamentally different.
A paradigm of psychosocial stress inhibits GnRH pulse amplitude. This effect is not reversed by treatment with RU486, a type II glucocorticoid receptor antagonist.
Regulation of Islet Hormone Release and Gastric Emptying by Endogenous Glucagon-Like Peptide 1 after Glucose Ingestion
Authors: Salehi Marzieh , Vahl Torsten P. , D'Alessio David A. 
Published: October 2008

Background: Exogenous administration of glucagon-like peptide (GLP)-1 improves glucose tolerance by stimulation of insulin secretion, inhibition of glucagon secretion, and delay of gastric emptying. It is not known which of these effects is involved in the action of endogenous GLP-1 to control blood glucose. To determine the role of endogenous GLP-1 on islet cell function and gastric emptying independent of variable glycemia, we clamped blood glucose before and during glucose ingestion with and without GLP-1 receptor blockade with exendin-[9–39] (Ex-9).
Methods: There were 10 healthy subjects that participated in two experiments each, one a control and one with infusion of 750 pm/kg · min Ex-9. Subjects consumed 75 g oral glucose solution mixed with d-xylose and 13C-glucose while their blood glucose levels were held fixed at approximately 8.9 mmol/liter.
Results: Plasma insulin levels during hyperglycemia alone were similar in the two studies (control, 282.5 ± 42 vs. Ex-9, 263.8 ± 59 pmol/liter) but were reduced by approximately 30% by Ex-9 after glucose ingestion (control, 1154 ± 203 vs. Ex-9, 835 ± 120 pmol/liter; P &lt; 0.05). Blocking the action of endogenous GLP-1 caused an approximate 80% increase in postprandial glucagon concentrations. The appearance of ingested d-xylose in the blood was not affected by Ex-9, suggesting that postprandial secretion of GLP-1 has only minimal effects on gastric emptying of oral glucose.
Conclusions: These findings indicate that GLP-1 is an incretin in healthy humans at modestly supraphysiological blood glucose levels. The primary effect of GLP-1 to regulate oral glucose tolerance is mediated by effects on islet hormones and not on gastric emptying.