bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effect of Repeated Stress Treatments During the Follicular Phase and Early Pregnancy on Reproductive Performance of Gilts
Authors: Soede NM , Roelofs JB , Verheijen RJE , Schouten WPG , Hazeleger W , Kemp B 
Published: January 2007

ContentsIn pig husbandry, stress is being considered an important cause of impaired reproductive performance. Therefore, an experiment was performed to quantify effects of repeated stressors during the follicular phase and/or during early pregnancy on reproductive performance of gilts. Eighty‐one cyclic gilts were assigned to one of four treatments, namely, stress treatment during the follicular phase (n = 20), stress treatment during early pregnancy (n = 20), stress treatment during both phases (n = 21) and no stress treatment (n = 20). All gilts were housed individually, but gilts in the stress treatments had no opportunity for visual or physical contact with other gilts. Further, animals in a stress‐treatment were grouped for half an hour at the start of the treatment and during the treatment period nose‐sling and an unpredictable feeding scheme were applied regularly. The extent of stress was monitored using heart rate measurements, behavioural observations and saliva cortisol levels during nose‐sling fixation. Of the 81 gilts, 93% showed oestrus and were inseminated. Of these, 93% were pregnant at day 35, having 17.9 ± 0.3 ovulations and 15.6 ± 0.3 foetuses. These parameters were not affected by treatment. The stress treatment during the follicular phase tended to shorten cycle length (stress: 20.8 ± 0.20; control: 21.2 ± 0.17 days, p = 0.07) and weight of foetuses at day 35 (stress: 4.47 ± 0.08 g; no stress: 4.69 ± 0.08 g, p = 0.06); stress during early pregnancy did not affect any of the reproduction parameters. Percentage stereotypic behaviour, heart rate and saliva cortisol levels varied greatly between animals and between days, but did not differ between the treatments. No relationships were found between any of the reproductive parameters and any of the stress parameters (heart rate, cortisol, stereotypic behaviour). These results indicate that the repeatedly applied acute stressors did not generate a chronic stress‐response and that these stressors during the follicular phase and/or during early pregnancy did not affect reproductive processes. It is not clear how these findings relate to suggested effects of stress(ors) on reproductive performance in pig husbandry.
Development of microsatellite markers for Dryobalanops aromatica (Dipterocarpaceae), a tropical emergent tree in Southeast Asia
Authors: NANAMI S. , IKEDA S. , TANI N. , TAN S. , DIWAY B. , HARADA K. , TSUMURA Y. , ITOH A. , YAMAKURA T. 
Published: January 2007

AbstractEight polymorphic microsatellite markers were developed in Dryobalanops aromatica, an emergent tree in tropical rain forests in Southeast Asia, using an enriched library method. For the assessment of microsatellite variation, 36 individuals from a natural population were analysed. The number of alleles per locus ranged from three to 16, with observed heterozygosity of 0.056–0.833 and expected heterozygosity of 0.054–0.882. These microsatellite markers will be useful for studies of population genetics, reproductive ecology and regeneration dynamics of D. aromatica.
Human hepatic progenitor cells express vasoactive intestinal peptide receptor type 2 and receive nerve endings
Authors: Cassiman David , Sinelli Nicoletta , Bockx Ilse , Vander Borght Sara , Petersen Bryon , De Vos Rita , Van Pelt Jos , Nevens Frederik , Libbrecht Louis , Roskams Tania 
Published: January 2007

AbstractBackground: We recently showed that human hepatic progenitor cells (HPCs) express muscarinic acetylcholine (Ach) receptor subtype 3 and that – following liver transplantation – HPC numbers are significantly reduced. To further elaborate on this, we examined whether HPC also express receptors for vasoactive intestinal peptide (VIP), which, besides Ach, also is an important parasympathetic neurotransmitter. VIP expressing nerves are known to be present in the liver.Methods: We performed immunohistochemistry for VIP receptor subtypes 1 and 2 (VIPR1 and 2), on sections of normal and diseased human liver (n=17), and double staining for VIPR2 and known HPC markers. We performed RT‐PCR for VIPR1 and 2 on total RNA from purified rat HPC. To document the probability of direct interaction, we also performed double immunostaining for nerve markers and HPC markers on human liver sections.Results: VIPR2 immunostaining was clearly positive in HPC and reactive bile ductules on paraffin‐embedded and frozen tissue sections. We could not demonstrate VIPR1 protein expression in the liver, with either of two VIPR1 antibodies tested. The presence of VIPR2 mRNA in HPC was confirmed by RT‐PCR. Nerve endings were shown to abut on reactive bile ductules.Conclusion: We show here for the first time that HPC express VIPR2 and receive nerve endings. These features, and the fact that HPC numbers are influenced by the presence or absence of the autonomic innervation of the liver, suggest a direct interaction.
Pseudoepitheliomatous hyperplasia formation after skin injury
Authors: Fu Xiaobing , Jiang Duying , Chen Wei , Sun, BS Tongzhou , Sheng Zhiyong 
Published: January 2007

ABSTRACTPseudoepitheliomatous hyperplasia (PEH) is characteristic of reactive epithelial downward proliferation into the dermis. To explore the mechanism of PEH formation, we investigated the cause, clinical characteristics, histopathologic change, and clinical treatment of PEH, the expression characteristics of stem cell factor (SCF), and its receptor c‐Kit in PEH and normal skin of PEH edge (PEH‐N). The clinical data of 11 patients with PEH were reviewed, and biopsy examination and bacterial cultures were performed. The histological features of PEH and expression levels of SCF, c‐Kit were examined with the pathological method and immunohistochemical methods. The results showed that in each case, histological examination revealed epidermal hyperplasia with irregular cords of epithelial cells extending into the dermis. The bacteria could be cultured and isolated from all PEH biopsies. These bacteria were resistant to several antibiotics, except vancomycin. Radical excision and daily dressing with vancomycin could cure PEH. SCF protein was expressed at stronger levels in sweat gland epithelial cells and interstitial cells of the PEH group vs. the PEH‐N group. c‐Kit was more strongly expressed by interstitial cells in PEH than in PEH‐N. It was concluded that the improper management of cutaneous wounds might cause PEH formation, which can be cured by surgical excision and administration of effective antibiotics. SCF and c‐Kit might be involved in the epidermal hyperplasia observed in PEH.
Responses of reactive astrocytes containing S100β protein and fibroblast growth factor‐2 in the border and in the adjacent preserved tissue after a contusion injury of the spinal cord in rats: implications for wound repair and neuroregeneration
Authors: Do Carmo Cunha Jinger , De Freitas Azevedo Levy Beatriz , De Luca Bianca Aparecida , De Andrade Michele Schultz Ramos , Gomide Vânia Canterucci , Chadi Gerson 
Published: January 2007

ABSTRACTThis paper demonstrates glial reaction and changes in the S100β protein and basic fibroblast growth factor (bFGF, FGF‐2) in the border and in the adjacent preserved tissue of the rat spinal cord after a contusion. In view of the expression of FGF‐2 and S100β in reactive glial cells and their ability to promote gliogenesis and neuronal trophism, the molecules have been considered to participate in the wound repair and regenerative events after nervous tissue injury. Adult rats were submitted to a moderate spinal cord (10th thoracic level) contusion induced by a New York University Impactor by dropping a 10 g rod from a distance of 25 mm onto the dorsal surface of the exposed dura spinal cord. Impactor curves and parameters were used to monitor the severity of the trauma. Control rats were submitted to sham operation. The motor behavioral spontaneous recovery was demonstrated by means of a BBB test and the combining behavior score up to 3 weeks after injury. Animals were killed 72 hours, 2, and 3 weeks after surgery and spinal cords were processed for immunohistochemistry to show glial fibrillary acidic protein positive astrocytes and OX‐42‐positive microglia/macrophages as well as changes in the S100β and FGF‐2 in the border and in the adjacent preserved tissue of the lesioned cords. The changes in the immunoreaction products were quantified by means of morphometric/microdensitometric image analysis, and the cell type expressing S100β and FGF‐2 was analyzed by means of two‐color immunofluorescence procedures. Massive increases of S100β and FGF‐2 were found in reactive astrocytes, not in reactive microglia, in the border and in the white and gray matters of adjacent preserved tissue of the contused spinal cord in the periods studied. The results are discussed in view of possible paracrine trophic actions of the reactive astrocytes, mediated by S100β and FGF‐2, triggering wound repair events in the border of the trauma, and also leading to neurotrophism and neuronal plasticity in the adjacent regions. These cellular and molecular responses may interfere with the pattern of behavioral recovery after a contusion injury of the spinal cord.
Impaired Emotional Facial Expression Recognition in Alcohol Dependence: Do These Deficits Persist With Midterm Abstinence?
Authors: Foisy Marie‐Line , Kornreich Charles , Fobe Anaïs , D'Hondt Laetitia , Pelc Isidore , Hanak Catherine , Verbanck Paul , Philippot Pierre 
Published: January 2007

Background: Emotional facial expression (EFE) decoding has been repetitively shown to be impaired in alcoholic inpatients. The present study aimed to replicate and extend previous findings on EFE recognition deficits in alcoholism.Methods: Alcoholic and control participants' performances were compared on an EFE decoding task with a transversal and a longitudinal design. More specifically, 49 alcoholic individuals were recruited at a long‐stay postdetoxification treatment center at the third or fourth week of their detoxification process. Twenty‐two of them [abstinent alcoholic participants (AA)] were met at the end of their hospitalization process, 2 months later. The 27 remaining patients [dropping alcoholic participants(AD)] dropped out from treatment before the second meeting. A control group (C) of 22 participants was constituted, and assessed twice with the same average time as AA between the 2 assessments. The 3 groups were similar regarding age, sex, and education level. Participants were presented at both times with an EFE decoding test consisting of 16 photographs depicting EFE of happiness, anger, disgust, and sadness.Results: The results corroborated previous findings highlighting more EFE decoding deficits in alcoholic participants compared with control participants, with no improvement after 3 months of abstinence. Transversal analyses further evidenced more EFE decoding difficulties in AD than in AA compared with controls.Conclusions: EFE decoding deficits in alcoholism persist with midterm abstinence. Alcoholic patients who dropped from treatment had the worst EFE decoding performance at baseline. Emotional facial expression decoding deficit could have a prognostic value in alcohol dependence.
Cognitive alterations in groups at risk for psychosis: neutral markers of genetic risk or indicators of social disability?
Authors: Jabben N. , Van Os J. , Janssen I. , Versmissen D. , Krabbendam L. 
Published: January 2007

Objective:  To investigate whether cognitive alterations associated with vulnerability to psychosis, are associated with expression of psychopathology and functional outcome in groups at different levels of risk for psychotic illness.Method:  Neurocognition, psychopathology and functional outcome were measured in subjects with variable risk for psychosis: i) 29 patients with psychotic disorder, ii) 46 subjects at familial risk, iii) 41 subjects at psychometric risk and iv) 54 control subjects.Results:  Dose‐response relationships between cognitive dysfunction and increasing risk for psychosis were found. Cognitive alterations were predicted by negative symptoms in patients and by positive psychotic experiences in the familial risk group. In both at risk groups, cognitive speed was associated with functional outcome.Conclusion:  Some cognitive impairments serve as neutral endophenotypic marker across the psychosis continuum. However, other cognitive alterations associated with transmission of psychosis may have a direct impact on the pathway from risk to psychopathology and alterations in functioning.
Predominant immature CD8α+ dendritic cells prevent graft‐vs.‐host disease but do not increase the risk of leukemia recurrence
Authors: Xu Lin , Duan Lianning , Cao Kaiyuan , Yuan Guangqing , Peng Yanwen , Huang Xiaorong , Xiang Peng , Li Shunong 
Published: January 2007

AbstractGraft‐vs.‐host disease (GVHD) remains the major limitation of allogeneic bone marrow transplantation (BMT) and stem cell transplantation, and leukemia recurrence is another important complication in leukemia treatment. Immature CD8α+ dendritic cells (DC) have good potential in GVHD treatment and immunological tolerance studies. To find a new way to prevent GVHD, not increasing the risk of leukemia recurrence, in this study, predominant CD8α+ immature DC were induced from murine bone marrow (BM) cells by 5 ng/mL granulocyte‐macrophage colony stimulating factor (GM‐CSF) plus 20‐ng/mL interleukin (IL)‐4, 100‐ng/mL stem cell factor (SCF) and 25‐ng/mL Flt3L, and 97.09 of prepared DC were CD8α+ on day 3. These DC were identified as morphologically and phenotypically immature CD8α+ DC. The suppressive function was observed in vitro, and then in vivo on allo‐BMT leukemia model. The prepared predominant immature CD8α+ DC were weak syngeneic lymphocyte stimulators and could suppress mixed leukocyte reaction in vitro. In vivo, they prevented the pathological changes of GVHD and prolonged the surviving time of allo‐BMT leukemia mice. The effect showed a dose–effect relationship. 86.7% of allo‐BMT plus 1 million predominant CD8α+ DC leukemia mice reached long‐term survival. Although predominant immature CD8α+ DC had the function of GVHD suppression, they did not increase leukemia recurrence. The method and findings may have important potency for GVHD treatment in clinical application.
Haematological characteristics of MYH9 disorders due to MYH9 R702 mutations
Authors: Kunishima Shinji , Yoshinari Miyako , Nishio Hisanori , Ida Komei , Miura Takuma , Matsushita Tadashi , Hamaguchi Motohiro , Saito Hidehiko 
Published: January 2007

Abstract Objective: MYH9 disorders are characterised by giant platelets, thrombocytopenia, and Döhle body‐like cytoplasmic granulocyte inclusion bodies that result from mutations in MYH9, the gene for non‐muscle myosin heavy chain‐IIA (NMMHC‐IIA). MYH9 R702 mutations are highly associated with Alport manifestations and result in Epstein syndrome. The aim of our study was to determine the haematological characteristics of MYH9 disorders as a result of R702 mutations to aid in making a proper diagnosis. Patients and methods: Platelet size of patients with MYH9 disorders was determined as platelet diameter by microscopic observation of 200 platelets on stained peripheral blood smears. Double in situ hybridisation using a biotinylated oligo(dT) probe and immunofluorescence analysis of neutrophil NMMHC‐IIA was performed on peripheral blood smears. Results: Patients carrying R702 mutations had significantly larger platelets than those with other MYH9 mutations. Although granulocyte inclusion bodies were mostly invisible on stained blood smears, immunofluorescence analysis for NMMHC‐IIA showed an abnormal type II localisation in all neutrophils. We first showed that poly(A)+ RNA coincided with accumulated NMMHC‐IIA at inclusion bodies in patients with MYH9 disorders. However, no condensation of poly(A)+ RNA at inclusion bodies was observed in patients with R702 mutations. Conclusion: Our study shows that R702 mutations result in especially large platelets and inclusion bodies being faint and mostly invisible on conventionally stained blood smears. We further demonstrated that poly(A)+ RNA content but not NMMHC‐IIA accumulation is responsible for the morphological appearance/stainability of inclusion bodies on stained blood smears and the amount of poly(A)+ RNA is decreased in those with R702 mutations.
Diffuse large B‐cell lymphoma arising independently to lymphoplasmacytic lymphoma: a case of two lymphomas
Authors: Sekikawa Tetsuaki , Takahara Shinobu , Suzuki Hideaki , Takeda Nobuakira , Yamada Hisashi , Horiguchi‐Yamada Junko 
Published: January 2007

AbstractRichter's syndrome occurs in 5–10% of patients with chronic lymphocytic leukemia, either by transformation of the primary neoplastic lymphocyte, or as a distinct B‐cell neoplasm. We report a Japanese patient with lymphoplasmacytic lymphoma in whom a diffuse large B‐cell lymphoma developed after treatment with rituximab. Molecular examination on immunoglobulin VH genes revealed that the lymphomas had arisen in two separate clones. We reviewed clinical case reports in literature, and found 30–40% of cases with Richter's syndrome and composite lymphoma had a second B‐cell lymphoma of a different origin.
Phenotypic and Genotypic Characterization of
Streptococcus pyogenes
Isolates Displaying the MLS
B
Phenotype of Macrolide Resistance in Spain, 1999 to 2005
Authors: Pérez-Trallero Emilio , Montes Milagrosa , Orden Beatriz , Tamayo Esther , García-Arenzana José M. , Marimón José M. 
Published: January 2007

ABSTRACT

The aim of this study was to describe the genetic characteristics of
Streptococcus pyogenes
showing the MLS
B
phenotype of macrolide resistance from 1999 to 2005 in Spain and to highlight the substantial increase in these isolates in the last few years. The antimicrobial susceptibilities of 17,232 group A streptococci isolated from Madrid and Gipuzkoa from 1999 to 2005 were studied. The presence of the resistance genes
ermA
,
ermB
,
mef
,
tetM
, and
tetO
and the presence of the
intTn
and
xis
genes of the Tn
916
-Tn
1545
transposon family were studied in a sample of 739 MLS
B
-resistant isolates. The epidemiological relationships among these isolates were analyzed by
emm
typing, T typing, and multilocus sequence typing. Erythromycin resistance was found in 21.3% of the isolates analyzed (annual variation of 14.3% to 28.9%). Until 2003, most erythromycin-resistant isolates showed the M phenotype, but in 2004 and 2005, about 50% of isolates showed the MLS
B
phenotype. Among the MLS
B
-resistant isolates studied, 16 clones were identified. The most prevalent clone was a strange
emm
11/T11/ST403 clone with a null
yqiL
allele. All but one of the 463
emm
11/T11/ST403 isolates carried the
ermB
,
tetM
,
intTn
, and
xis
genes. The second most prevalent MLS
B
-resistant clone was
emm
28/T28/ST52, which comprised two subclones: one bacitracin-resistant, tetracycline-susceptible subclone carrying the
ermB
gene (
n
= 115) and another bacitracin-susceptible, tetracycline-resistant subclone carrying the
ermB
and
tetM
genes (
n
= 33). The rapid diffusion of these two clones, and especially of
emm
11/T11/ST403, caused the large increase in MLS
B
-resistant
S. pyogenes
isolates in Spain, suggesting a potential ability for international dissemination.
Lack of Relationship between Purine Biosynthesis and Vancomycin Resistance in
Staphylococcus aureus
: a Cautionary Tale for Microarray Interpretation
Authors: Fox Paige M. , Climo Michael W. , Archer Gordon L. 
Published: January 2007

ABSTRACT

Previous microarray data (E. Mongodin, J. Finan, M. W. Climo, A. Rosato, S. Gill, and G. L. Archer, J. Bacteriol. 185:4638-4643, 2003) noted an association in two vancomycin-intermediate
Staphylococcus aureus
(VISA) strains between high-level, passage-induced vancomycin resistance, a marked increase in the transcription of purine biosynthetic genes, and mutation of the putative purine regulator
purR
. Initial studies to report on the possible association between vancomycin resistance and alterations in purine metabolism in one of these strains (VP-32) confirmed, by Western analysis, an increase in the translation of PurH and PurM, two purine pathway enzymes. In addition, PurR was identified, by knockout and complementation in a vancomycin-susceptible strain, as a repressor of the purine biosynthetic operon in
S. aureus
, and the PurR missense mutation was shown to inactivate the repressor. However, despite the apparent relationship between increased purine biosynthesis and increased vancomycin resistance in VP-32, neither the addition of exogenous purines to a defined growth medium nor the truncation or inactivation of
purR
improved the growth of vancomycin-susceptible
S. aureus
in the presence of vancomycin. Furthermore, the passage of additional vancomycin-susceptible and VISA strains to high-level vancomycin resistance occurred without changes in cellular purine metabolism or mutation of
purR
despite the development of thickened cell walls in passaged strains. Thus, we could confirm neither a role for altered purine metabolism in the development of vancomycin resistance nor its requirement for the maintenance of a thickened cell wall. The failure of biochemical and physiological studies to support the association between transcription and phenotype initially found in careful microarray studies emphasizes the importance of follow-up investigations to confirm microarray observations.
First Linezolid-Resistant Clinical Isolates of
Mycobacterium tuberculosis
Authors: Richter Elvira , Rüsch-Gerdes Sabine , Hillemann Doris 
Published: January 2007

ABSTRACT

Linezolid resistance was found in 4 (1.9%) of 210 multidrug-resistant
Mycobacterium tuberculosis
strains. The MICs of linezolid were 4 μg/ml (one strain) and 8 μg/ml (three strains). Since no mutations were detected in potential target genes, the mechanism of resistance remains unclear.
A Mycobacterial Gene Involved in Synthesis of an Outer Cell Envelope Lipid Is a Key Factor in Prevention of Phagosome Maturation
Authors: Robinson Nirmal , Wolke Martina , Ernestus Karen , Plum Georg 
Published: January 2007

ABSTRACT

Virulent mycobacteria cause arrest of phagosome maturation as a part of their survival strategy in hosts. This process is mediated through multiple virulence factors, whose molecular nature remains elusive. Using
Mycobacterium marinum
as a model, we performed a genome-wide screen to identify mutants whose ability to inhibit phagosome maturation was impaired, and we succeeded in isolating a comprehensive set of mutants that were not able to occupy an early endosome-like phagosomal compartment in mammalian macrophages. Categorizing and ordering the multiple mutations according to their gene families demonstrated that the genes modulating the cell envelope are the principal factors in arresting phagosome maturation. In particular, we identified a novel gene,
pmiA
, which is capable of influencing the constitution of the cell envelope lipids, thereby leading to the phagosome maturation block. The
pmiA
mutant was not able to resist phagosome maturation and was severely attenuated in mice. Complementing the mutant with the wild-type gene restored the attenuated virulence to wild-type levels in mice.