bluuebunny/crossref_metadata_2025_split huggingface dataset:
In vitroEvaluation ofin vivoFertilizing Ability of Frozen Rabbit Semen
Authors: Viudes‐de‐Castro MP , Mocé E , Vicente JS , Marco‐Jiménez F , Lavara R 
Published: March 2005

ContentsThe present work studied different spermatozoa parameters and the ability of frozen rabbit spermatozoa to fertilize,in vitro,in vivo‐matured oocytes, as a test to predict theirin vivofertility and prolificacy. Semen from rabbit bucks was frozen using two freezing protocols [in a freezer at −30°C or in liquid nitrogen vapour (LNV)]. For thein vivotrial, females were inseminated with frozen‐thawed spermatozoa. Oocytes used forin vitrotesting were recovered 14 h after ovulation induction from donors and co‐incubated with 2 × 106frozen‐thawed spermatozoa during 4 h at 37°C in Tyrode's medium under an atmosphere of 5% CO2in air with maximal humidity. After co‐incubation period, presumptive zygotes were cultured in TCM199 supplemented with 20% foetal bovine serum (FBS), under the same conditions described above. Although no statistical differences were observed between freezing protocols in seminal parameters [motility rate: 40 and 35%, VCL: 35 and 46 μm/s, amplitude of lateral head displacement (ALH): 1.7 and 2.4 μm, for semen frozen at −30°C and in LNV, respectively], significant differences were noted in the fertilizing abilityin vivoandin vitro. Semen frozen at −30°C showed the highest fertilizing abilityin vitro(26.7% vs 6.2 and 8.7% for semen frozen at −30°C, in LNV and fresh semen, respectively) and the lowest fertility ratein vivo(21.7% vs 64.2% and 70.6% for semen frozen at −30°C, in LNV and fresh semen, respectively). Sperm frozen at −30°C seemed to be more capacitated.
Free Oestrone in Adipose Tissue and its Relation to Androstenone and Skatole in Entire Male Pigs
Authors: Zamaratskaia G , Madej A , Babol J , Squires EJ , Lundström K 
Published: March 2005

ContentsRelationship between free oestrone and boar taint compounds in adipose tissue were studied in two groups of entire male pigs of different breeds. Group A consisted of 33 entire crossbred male pigs (dam Yorkshire and sire backcross Yorkshire × Wild Boar, generation seven). Group B consisted of 194 entire male pigs of crossbreeds between Swedish Hampshire (H) and Finnish Landrace (L), LH × H, H × LH, LH × LH (dam × sire). The measurements of free oestrone in adipose tissue were performed with a new method developed and validated in our laboratories. The standard curve was linear for concentrations of free oestrone ranging from 0.13 to 5.10 ng/g. The method exhibited parallelism of results between serial dilutions and a mean recovery of 97 ± 13.7%. Intra‐assay variations for samples with concentrations of free oestrone from 0.67 to 2.08 ng/g were from 9.23 to 11.94%. Inter‐assay variations for the samples with concentrations of free oestrone from 0.89 to 2.96 ng/g were from 3.78 to 10.11%. The levels of free oestrone in fat from group A were well correlated with fat levels of androstenone (r = 0.66; p < 0.001) and levels of oestrone sulphate in peripheral plasma collected at the same time as the fat (r = 0.74, p < 0.001). The levels of free oestrone in fat from group B were significantly correlated to fat levels of androstenone (r = 0.68, p < 0.001) and skatole (r = 0.29, p < 0.001). In group B, age‐related differences in fat levels of free oestrone, androstenone and skatole were studied. Free oestrone and skatole levels increased simultaneously at the age of 22 week (p < 0.05 for both), and androstenone levels increased at the age of 26 week (p < 0.05). It was suggested that the levels of free oestrone in adipose tissue might be used for the evaluation of hormonal status of male pigs as an alternative to plasma levels of testicular hormones. The levels of free oestrone might be involved in the regulation of skatole levels in fat as indicated by both the simultaneous increases in skatole and free oestrone levels in fat and positive correlation between skatole and free oestrone.
Effects of baroreceptor stimulation and opioids on the auditory startle reflex
Authors: Nyklíc̆ek Ivan , Wijnen Viona , Rau Harald 
Published: March 2005

AbstractWe examined (a) whether carotid baroreceptor stimulation attenuates the auditory startle response and its modulation by preceding affective pictures, and (b) whether these effects are mediated by endogenous opioids. Seventy‐eight young normotensive adults with or without a parental history of hypertension received brief exposures to affective pictures and noise bursts during phasic manipulation of the carotid baroreceptors. In each participant, opioids were blocked by naltrexone in half of the sessions. Baroreceptor stimulation had a strong dampening effect on the startle response. This effect was not influenced by opioid blockade, sex, or parental history of hypertension. No baroreceptor effects were obtained regarding ratings of the affective pictures or startle modulation by the pictures. The baroreceptor stimulation effects seem to be mediated by the basal primary acoustic startle circuit rather than by higher affective circuits.
Paradoxal effect of salbutamol in an in vitro model of bronchoprotection
Authors: Girodet P.O. , Berger P. , Martinez B. , Marthan R. , Advenier C. , Molimard M. 
Published: March 2005

AbstractSalbutamol‐induced hyperresponsiveness to acetylcholine was investigated in human and guinea‐pig isolated airways and cultured human airway smooth muscle cells. Salbutamol (10−7–10−5 m) inhibited contractions induced by low concentrations of acetylcholine (10−8–10−7 m) but potentiated contractions induced by higher concentrations of acetylcholine (10−5–10−3 m). Pretreatment with the calcium channel antagonist nicardipine suppressed salbutamol‐induced hyperresponse. Stimulation of cultured human airway smooth muscle cells with salbutamol (10−6 m) amplified intracellular calcium concentration rise induced by acetylcholine (10−5 m). Propranolol (10−7 m), a β1‐ and β2‐adrenoceptor antagonist, and ICI 118551 (10−7–10−6 m), a β2‐adrenoceptor antagonist, suppressed the inhibitory effect of salbutamol but did not inhibit the hyperresponse on high concentrations of acetylcholine. In contrast, higher concentration of propranolol (10−6 m) inhibited salbutamol‐induced hyperreactivity. Effects of salbutamol were not affected by atenolol, a β1‐adrenoceptor blocker. Salbutamol‐induced hyperresponsiveness is mediated through a mechanism involving calcium channel activation.
Taurine treatment protects against chronic nicotine‐induced oxidative changes
Authors: Şener Göksel , Özer Şehirli A. , İpçi Yeşim , Çetinel Şule , Cikler Esra , Gedik Nursal , Alican İnci 
Published: March 2005

AbstractExperiments have shown that chronic nicotine administration caused oxidative damage in various organs by increasing lipid peroxidation products and decreasing the activity of endogenous antioxidants. The aim of this study was to investigate the effects of taurine treatment on nicotine‐induced oxidative changes in rat thoracic aorta and heart and to explore the possible mechanisms of action. Male Wistar albino rats (200–250 g) were injected with nicotine hydrogen bitartrate (0.6 mg/kg; i.p.) or saline for 21 days. Taurine was administered (50 mg/kg; i.p.) alone or along with nicotine injections. After decapitation, the thoracic aorta and heart tissues were excised. The aorta was used for in vitro contractility studies or stored along with the heart samples for the measurement of malondialdehyde (MDA) and glutathione (GSH) levels, myeloperoxidase (MPO) activity and collagen content. Tissue samples were also examined histologically. Serum samples were stored for the measurement of MDA, GSH and lactate dehydrogenase (LDH) activity. Chronic nicotine treatment impaired both the contraction and relaxation responses of the aortic rings to phenylephrine and acetylcholine, respectively. It increased lipid peroxidation, MPO levels and tissue collagen content of both aorta and heart samples. Taurine supplementation to nicotine‐treated animals reversed the contractile dysfunction and restored the endogenous GSH levels and decreased high lipid peroxidation and MPO activities in both tissues. These data suggest that taurine supplementation effectively attenuates the oxidative damage because of chronic nicotine administration possibly by its antioxidant effects.
DORSAL PENTAGONAL ISLAND FLAP: A TECHNIQUE OF WEB RECONSTRUCTION FOR SYNDACTYLY THAT FACILITATES DIRECT CLOSURE
Authors: Teoh L. C. , Lee J. Y. L. 
Published: March 2005

Though many techniques have been described for the correction of syndactyly, current methods result in skin deficiency that requires skin grafting, especially at the finger bases. We discuss the technical aspects and document our experience with the dorsal pentagonal metacarpal island flap for reconstruction of the web commissure in a series of 12 patients (22 webs) with syndactyly of varying complexity. In appropriately selected cases, this technique can improve reconstruction of the web commissure, facilitating direct closure, minimising the need for skin grafts and offers the potential for continued growth. This reduces operative time significantly and simplifies post-operative wound care. In this series, all our cases healed primarily in two to three weeks with minimal donor site morbidity. There were no post-operative complications, although the prominent dorsal scar remains a concern. At an average follow-up of 33.7 months, no cases of contracture or web creep after correction were noted.
Loss of Runx1 perturbs adult hematopoiesis and is associated with a myeloproliferative phenotype
Authors: Growney Joseph D. , Shigematsu Hirokazu , Li Zhe , Lee Benjamin H. , Adelsperger Jennifer , Rowan Rebecca , Curley David P. , Kutok Jeffery L. , Akashi Koichi , Williams Ifor R. , Speck Nancy A. , Gilliland D. Gary 
Published: March 2005

AbstractHomozygous loss of function of Runx1 (Runt-related transcription factor 1 gene) during murine development results in an embryonic lethal phenotype characterized by a complete lack of definitive hematopoiesis. In light of recent reports of disparate requirements for hematopoietic transcription factors during development as opposed to adult hematopoiesis, we used a conditional gene-targeting strategy to effect the loss of Runx1 function in adult mice. In contrast with the critical role of Runx1 during development, Runx1 was not essential for hematopoiesis in the adult hematopoietic compartment, though a number of significant hematopoietic abnormalities were observed. Runx1 excision had lineage-specific effects on B- and T-cell maturation and pronounced inhibition of common lymphocyte progenitor production. Runx1 excision also resulted in inefficient platelet production. Of note, Runx1-deficient mice developed a mild myeloproliferative phenotype characterized by an increase in peripheral blood neutrophils, an increase in myeloid progenitor populations, and extramedullary hematopoiesis composed of maturing myeloid and erythroid elements. These findings indicate that Runx1 deficiency has markedly different consequences during development compared with adult hematopoiesis, and they provide insight into the phenotypic manifestations of Runx1 deficiency in hematopoietic malignancies.
NK-dependent DC maturation is mediated by TNFα and IFNγ released upon engagement of the NKp30 triggering receptor
Authors: Vitale Massimo , Chiesa Mariella Della , Carlomagno Simona , Pende Daniela , Aricò Maurizio , Moretta Lorenzo , Moretta Alessandro 
Published: March 2005

Abstract
Natural killer (NK) cells were recently shown to play a relevant role in the process of dendritic cell (DC) maturation. This function is exerted either by direct DC stimulation or through killing those DCs that did not properly acquire a mature phenotype. While killing of immature DCs is dependent on the function of the NKp30 triggering receptor, the mechanism by which NK cells induce DC maturation is still unclear. In this study, we show that also the NK-mediated induction of DC maturation is dependent on NKp30. Upon NK/DC interaction, resulting in NKp30 engagement, NK cells produced tumor necrosis factor α (TNFα) (and interferon γ [IFNγ]) that, in turn, promoted DC maturation. Masking of NKp30 with specific monoclonal antibodies (mAbs) strongly reduced maturation of DCs cocultured with NK cells. In addition, supernatant from NK cells stimulated via NKp30 induced DC maturation, and this effect was neutralized by anti-TNFα antibodies (Abs). This NKp30 function is controlled by the HLA-specific inhibitory NK receptors. Accordingly, the ability to promote maturation was essentially confined to NK cells expressing the killer immunoglobulin-like receptor–negative (KIR–) NKG2Adull phenotype. Finally, the analysis of perforin-deficient NK cells allowed the dissection of the 2 NKp30-mediated NK-cell functions, since NKp30 could induce cytokine-dependent DC maturation in the absence of NK-mediated DC killing.
The antitumor immune response in HER-2 positive, metastatic breast cancer patients
Authors: Juranic Zorica D , Neskovic-Konstantinovic Zora , Stanojkovic Tatjana P , Zizak Zeljko , Srdic Tatjana , Stanojevic-Bakic Nevenka , Milosevic Dusanka , Jovanovic Danica 
Published: March 2005

AbstractThe aim of this study was to determine the basis for anti-tumor immune reactivity observed in patients with human epidermal growth factor receptor-2 (HER-2) (3+) breast carcinoma using an in vitro model in which the role of the HER-2-specific monoclonal antibody Herceptin was also investigated. Patients with metastatic breast cancer who had their primary tumor resected were included in this study. Peripheral blood mononuclear cell (PBMC)-dependent cytotoxicity in the presence or absence of Herceptin were assessed using the survival of target breast adenocarcinoma MDA-MB-361 cells as a parameter in a (3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) test. We observed a significant increase in PBMC-dependent cytotoxicity when autologous serum was introduced in the assay. Furthermore, the addition of Herceptin significantly increases their cytotoxicity. These data suggest that autologous serum constitutively contains factors that might affect PBMC-dependent cytotoxic activity against HER-2 positive cancer cells.
Modulation of macrophage functions by sheeppox virus provides clues to understand interaction of the virus with host immune system
Authors: Abu-EL-Saad Abdel-Aziz S , Abdel-Moneim Ahmed S 
Published: March 2005

Abstract

Background
Poxviruses encode a range of immunomodulatory genes to subvert or evade the challenges posed by the innate and adaptive immune responses. However, the inactivated poxviruses possessed immunostimulating capacity and were used as a prophylactic or metaphylactic application that efficiently reduced susceptibility to infectious diseases in different species. This fact is intensively studied in different genera of poxviruses. However, little is known about the basic mechanisms adopted by sheeppox virus (SPPV). SPPV causes an acute disease of sheep that recently, has been observed to reinfect its host in spite of vaccination.

Results
By injecting inactivated or attenuated sheeppox virus SPPV vaccine in adult male Swiss mice, SPPV was found to reduce macrophages' functions in a local event that occurs at the site of application 12 h after vaccine administration as indicated by increased level of IL-10 and decreased level of SOD from cultured peritoneal macrophages. In contrast increased levels of IL-12, and SOD activity from cultured splenic macrophages, lymphocyte response to PHA-P, and in-vivo response to T-dependant Ag were detected. These effects were observed in both attenuated and inactivated SPPV, but more prominent in attenuated one.

Conclusion
The results of this study help to elucidate, the phenomenon of existence natural SPPV infections in sheep instead of vaccination and the basic mechanisms responsible for the immunostimulating capacity of sheeppox virus. Locally, SPPV shows evidence for an immune escape mechanism that alleviates the host's immune response. Later and systemically, the virus protects the host from any fatal consequences of the immune system suppression.
NACA is a positive regulator of human erythroid-cell differentiation
Authors: Lopez Sophie , Stuhl Laetitia , Fichelson Serge , Dubart-Kupperschmitt Anne , St Arnaud René , Galindo Jean-Rémy , Murati Anne , Berda Nicole , Dubreuil Patrice , Gomez Sophie 
Published: March 2005

We have previously identified the transcript encoding NACA (the α chain of the nascent-polypeptide-associated complex) as a cytokine-modulated specific transcript in the human TF-1 erythroleukemic cell line. This protein was already known to be a transcriptional co-activator that acts by potentiating AP-1 activity in osteoblasts, and is known to be involved in the targeting of nascent polypeptides. In this study, we investigate the role of NACA in human hematopoiesis.
Protein distribution analyses indicate that NACA is expressed in undifferentiated TF-1 cells and in human-cord-blood-derived CD34+ progenitor cells. Its expression is maintained during in vitro erythroid differentiation but, in marked contrast, its expression is suppressed during their megakaryocytic or granulocytic differentiation. Ectopic expression of NACA in CD34+ cells under culture conditions that induce erythroid-lineage differentiation leads to a marked acceleration of erythroid-cell differentiation. Moreover, ectopic expression of NACA induces erythropoietin-independent differentiation of TF-1 cells, whereas downregulation of NACA by RNA interference abolishes the induction of hemoglobin production in these cells and diminishes glycophorin-A (GPA) expression by CD34+ progenitors cultured under erythroid differentiation conditions. Altogether, these results characterize NACA as a new factor involved in the positive regulation of human erythroid-cell differentiation.
Phosphorylation-Dependent Low-Frequency Depression at Phasic Synapses of a Crayfish Motoneuron
Authors: Silverman-Gavrila Lorelei B. , Orth Peter M. R. , Charlton Milton P. 
Published: March 2005

Extremes in presynaptic differentiation can be studied at the crayfish leg extensor muscle where, on the same muscle fiber, one motoneuron makes “phasic” depressing synapses that have a high probability of neurotransmitter release and another motoneuron makes “tonic,” low-probability, facilitating synapses. The large motor axons permit intracellular access to presynaptic sites. We examined the role of phosphorylation during low-frequency depression (LFD) in the relatively little studied phasic synapses.LFD occurs with stimulation at 0.2 Hz and develops with time constants of 4 and 105 min to reach >50% depression of transmitter release in 60 min similar to long-term depression in mammals. LFD is not associated with changes in postsynaptic sensitivity to transmitter and thus is a presynaptic event, although it is not accompanied by changes in the presynaptic action potential. Blockade of protein kinases accelerated the slow phase of LFD, but stimulation of kinases reduced depression. Blockade of protein phosphatases 1A/2A reversed the slow phase. When calcineurin was inhibited, both phases of LFD were abolished, and facilitation occurred instead. Immunostaining showed calcineurin-like immunoreactivity in synaptic terminals. Recovery from LFD occurred in ∼1 h if stimulation frequency was reduced to 0.0016 Hz. Recovery was blocked by kinase inhibition.This study shows that phosphorylation-dependent mechanisms are involved in LFD and suggests that exocytosis is controlled by conditions that shift the balance between phosphorylated and unphosphorylated substrates. The shift can occur by alteration in the relative activities of protein kinases and phosphatases.
Closure of a moderately large atrial septal defect with a self‐fabricated fenestrated Amplatzer septal occluder in an 85‐year‐old patient with reduced diastolic elasticity of the left ventricle
Authors: Holzer Ralf , Cao Qi‐Ling , Hijazi Ziyad M. 
Published: March 2005

AbstractPercutaneous closure of an atrial septal defect (ASD) in the elderly with reduced diastolic elasticity of the left ventricle poses a significant management challenge. We report on the case of an 85‐year‐old patient who was admitted for percutaneous device closure of a moderately large secundum atrial septal defect. Hemodynamic evaluation documented an increase in left atrial pressure from a mean of 12 mm Hg to a mean of 32 mm Hg after balloon test occlusion of the ASD. Two months later, after adequate pretreatment with diuretics and afterload‐reducing substances, he underwent successful closure of the ASD using a self‐fabricated fenestrated Amplatzer septal occluder, which resulted in a postimplantation left atrial pressure of a mean of 18 mm Hg. Recovery was unremarkable and the fenestration has remained patent for 3 months since implantation of the device. This unique case highlights the feasibility of using a self‐fabricated fenestrated Amplatzer septal occluder to close interatrial communications in elderly patients with diastolic dysfunction of the left ventricle. Catheter Cardiovasc Interv 2005;64:513–518. © 2005 Wiley‐Liss, Inc.
Renal failure after percutaneous coronary intervention is associated with high mortality
Authors: Gupta Ritesh , Gurm Hitinder S. , Bhatt Deepak L. , Chew Derek P. , Ellis Stephen G. 
Published: March 2005

AbstractRenal failure is a marker of poor outcome in the general population. Renal failure after percutaneous coronary artery intervention (PCI) is associated with an increased hazard of in‐hospital mortality. We hypothesized that post‐PCI renal insufficiency would be a predictor of long‐term mortality in patients undergoing PCI who survive for over 30 days after the procedure. A retrospective analysis was conducted from a registry of 9,067 patients undergoing PCI at our center from 1997 to 2001. A rise in creatinine by 1 mg/dl from baseline was defined as post‐PCI renal insufficiency. Vital status was assessed using Social Security Death Index. There were a total of 996 deaths over a mean follow‐up period of 3.2 years. In a multivariate analysis, history of recent acute myocardial infarction, older age, insulin‐dependent diabetes, baseline creatinine greater than 1.5 mg/dl, and presence of mitral regurgitation were associated with post‐PCI renal insufficiency. Developing post‐PCI renal insufficiency was associated with a 4.31‐fold hazard of mortality in univariate analysis and a 1.77‐fold hazard after adjustment for known predictors of mortality after PCI. The 1‐year survival in patients with renal failure was 70.3% ± 3.91%, compared to a survival of 93.6% ± 0.27% in those without any post‐PCI renal insufficiency (P < 0.0001). Acute renal insufficiency after PCI is a strong and independent predictor of long‐term mortality in patients who survived for 30 days after the procedure. Catheter Cardiovasc Interv 2005;64:442–448. © 2005 Wiley‐Liss, Inc.