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1.
Kamiel Spoelstra Serge Daan 《Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology》2008,194(3):235-242
Mutations in each of the genes mPer1, mPer2, mCry1 and mCry2 separately cause deviations from the wild type circadian system. Differences between these mutant strains have inspired the
hypothesis that the duality of circadian genes (two mPer and two mCry genes involved) is related to the existence of two components in the circadian oscillator (Daan et al., J Biol Rhythms 16:105–116,
2001). We tested the predictions from this theory that the circadian period (τ) lengthens under constant illumination (LL)
in mCry1 and mPer1 mutant mice, while it shortens in mCry2 and mPer2 mutants. mCry1
−/−
and mCry2
−/−
knockout mice both consistently increased τ with increasing light intensity, as did wild type mice. With increasing illumination,
rhythmicity is reduced in mCry1, mCry2 and mPer1, but not in mPer2 deficient mice. Results for mPer mutant mice are in agreement with data reported on these strains earlier by Steinlechner et al. (J Biol Rhythms 17:202–209,
2002), and also with the predictions from the model. The increase in cycle length of the circadian system by light in the
mCry2 deficient mice violates the predictions. The model is thereby rejected: the mCry genes do not play a differential role, although the opposite responses of mPer mutants to light remain consistent with a functional Evening–Morning differentiation. 相似文献
2.
Increased 5-HT3-mediated signalling in pelvic afferent neurons from mice deficient in P2X2 and/or P2X3 receptor subunits 总被引:1,自引:0,他引:1
Extracellular ATP and 5-hydroxytryptamine (5-HT) are both involved in visceral sensory pathways by interacting with P2X and 5-HT3 receptors, respectively. We have investigated the changes in P2X and 5-HT3-mediated signalling in pelvic afferent neurons in mice deficient in P2X2 and/or P2X3 subunits by whole-cell recording of L6–S2 dorsal root ganglion (DRG) neurons and by multi-unit recording of pelvic afferents of the colorectum. In wildtype DRG neurons, ATP evoked transient, sustained or mixed (biphasic) inward currents. Transient currents were absent in P2X3
−/− neurons, whereas sustained currents were absent in P2X2
−/− DRG neurons. Neither transient nor sustained currents were observed following application of ATP or α,β-methylene ATP (α,β-meATP) in P2X2/P2X3
Dbl−/− DRG neurons. 5-HT was found to induce a fast inward current in 63% of DRG neurons from wildtype mice, which was blocked by tropisetron, a 5-HT3 receptor antagonist. The percentage of DRG neurons responding to 5-HT was significantly increased in P2X 2
−/−, P2X3
−/− and P2X2/P2X3
Dbl−/− mice, and the amplitude of 5-HT response was significantly increased in P2X2/P2X3
Dbl−/− mice. The pelvic afferent response to colorectal distension was attenuated in P2X2/P2X3
Dbl−/− mice, but the response to serosal application of 5-HT was enhanced. Furthermore, tropisetron resulted in a greater reduction in pelvic afferent responses to colorectal distension in the P2X2/P2X3
Dbl−/− preparations. These data suggest that P2X receptors containing the P2X2 and/or P2X3 subunits mediate purinergic activation of colorectal afferents and that 5-HT signalling in pelvic afferent neurons is up-regulated in mice lacking P2X2 or P2X3 receptor genes. This effect is more pronounced when both subunits are absent. 相似文献
3.
Jiang-guo Zhang Xiao-min Qin Xiao-jing Wang Wei-ming Yan Chuan-long Zhu Xiao-ping Luo Qin Ning 《中国病毒学》2007,22(5):339-346
To study the contribution of T cell subsets in the pathogenesis of Murine hepatitis virus Type 3 (MHV-3) induced chronic viral
hepatitis in C3H/Hej mice, ninety C3H/Hej mice were chosen to individually receive 10 plaque forming units (PFU) of MHV-3
intraperitoneally. The changes of virus titer and pathology in liver tissue were examined by standard plaque assay and by
the hematoxylin/eosin (HE) staining method from 2 days post MHV-3 infection. The ratios of T cell subsets including CD3+CD4+CD8−, CD3+CD4−CD8+, CD3+CD4−CD8−, CD3+CD4+CD25+, CD3+CD4+CD25− and CD3+ CD4−CD25+ T lymphocyte of total T lymphocytes in blood, spleen and liver were examined at 0, 2, 4, 6, 8, 10, 12, 15, 20, 25, 30, 40
days post MHV-3 infection by flow cytosorting. We observed that the virus titer raised and showed persistent virus duplications
and inflammatory changes in the livers of C3H/Hej mice from 2 days post MHV-3 infection. The double negative T cell (DN Treg
cell) and CD4+CD25+ T cell ratios increased significantly from 2 days post MHV-3 infection in C3H/Hej mice, and CD3+CD4+CD8−, CD3+CD4−CD8+, CD3+CD4+CD25− and CD3+CD4−CD25+ T cell ratios decreased accordingly. In conclusion, the changes of virus titer and pathology in the livers of C3H/Hej mice
post MHV-3 suggest their contribution to viral persistence. Further characterizations of DN Treg cells are that infection
indicates that MHV-3 could induce the chronic inflammation in livers of C3H/Hej mice. The increase of the DN Treg cell and
CD4+CD25+ T cell ratios in C3H/Hej mice post MHV-3 infection suggests that DN Treg cells and CD4+CD25+ T cells may both have important suppressive immunomodulation functions in the development of chronic viral hepatitis and
have important roles in the virus persistent infection. Further characterizations of DNT cell and CD4+CD25+ T cell are under investigation.
Foundation items: National Nature Science Foundation (30571643, 30672380), Major State Basic Research Development Program
of China (2005CB522901, 2007CB512904) 相似文献
4.
Apoptosis has been implicated in mediating denervation-induced muscle wasting. In this study we determined the effect of interference
of apoptosis on muscle wasting during denervation by using mice genetically deficient in pro-apoptotic Bax. After denervation,
muscle wasting was evident in both wild-type and Bax−/− muscles but reduction of muscle weight was attenuated in Bax−/− mice. Apoptotic DNA fragmentation increased in wild-type denervated muscles whereas there was no statistical increase in
DNA fragmentation in denervated muscles from Bax−/− mice. Mitochondrial AIF and Smac/DIABLO releases and Bcl-2, p53 and HSP27 increased whereas XIAP and MnSOD decreased to a
similar extent in muscles from wild-type and Bax−/− mice following denervation. Mitochondrial cytochrome c release was elevated in denervated muscles from wild-type mice but the increase was suppressed in muscles from Bax−/− mice. Increases in caspase-3 and -9 activities and oxidative stress markers H2O2, MDA/4-HAE and nitrotyrosine were all evident in denervated muscles from wild-type mice but these changes were absent in
muscles from Bax−/− mice. Moreover, ARC increased exclusively in denervated Bax−/− muscle. Our data indicate that under conditions of denervation, pro-apoptotic signalling is suppressed and muscle wasting
is attenuated when the Bax gene is lacking. These findings suggest that interventions targeting apoptosis may be valuable
in ameliorating denervation-associated pathologic muscle wasting in certain neuromuscular disorders that involve partial or
full denervation. 相似文献
5.
Guenterberg KD Lesinski GB Mundy-Bosse BL Karpa VI Jaime-Ramirez AC Wei L Carson WE 《Cancer immunology, immunotherapy : CII》2011,60(9):1281-1288
Interferon-alpha (IFN-α) is an immunomodulatory cytokine that is used clinically for the treatment of melanoma in the adjuvant
setting. The cellular actions of IFN-α are regulated by the suppressors of cytokine signaling (SOCS) family of proteins. We
hypothesized that the anti-tumor activity of exogenous IFN-α would be enhanced in SOCS1-deficient mice. SOCS1-deficient (SOCS1−/−) or control (SOCS1+/+) mice on an IFN-γ−/− C57BL/6 background bearing intraperitoneal (i.p.) JB/MS murine melanoma cells were treated for 30 days with i.p. injections
of IFN-A/D or PBS (vehicle). Log-rank Kaplan-Meier survival curves were used to evaluate survival. Tumor-bearing control SOCS1+/+ mice receiving IFN-A/D had significantly enhanced survival versus PBS–treated mice (P = 0.0048). The anti-tumor effects of IFN-A/D therapy were significantly enhanced in tumor-bearing SOCS1−/− mice; 75% of these mice survived tumor challenge, whereas PBS-treated SOCS1−/− mice all died at 13-16 days (P = 0.00038). Antibody (Ab) depletion of CD8+ T cells abrogated the anti-tumor effects of IFN-A/D in SOCS1−/− mice as compared with mice receiving a control antibody (P = 0.0021). CD4+ T-cell depletion from SOCS1−/− mice also inhibited the effects of IFN-A/D (P = 0.0003). IFN-A/D did not alter expression of CD80 or CD86 on splenocytes of SOCS1+/+ or SOCS1−/− mice, or the proportion of T regulatory cells or myeloid-derived suppressor cells in SOCS1+/+ or SOCS1−/− mice. An analysis of T-cell function did reveal increased proliferation of SOCS1-deficient splenocytes at baseline and in
response to mitogenic stimuli. These data suggest that modulation of SOCS1 function in T-cell subsets could enhance the anti-tumor
effects of IFN-α in the setting of melanoma. 相似文献
6.
Taylor JR Whittamore JM Wilson RW Grosell M 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》2007,177(6):597-608
The effects of feeding on both acid–base and ion exchange with the environment, and internal acid–base and ion balance, in
freshwater and seawater-acclimated flounder were investigated. Following voluntary feeding on a meal of 2.5–5% body mass and
subsequent gastric acid secretion, no systemic alkaline tide or respiratory compensation was observed in either group. Ammonia
efflux rates more than doubled from 489 ± 35 and 555 ± 64 μmol kg−1 h−1 under control conditions to 1,228 ± 127 and 1,300 ± 154 μmol kg−1 h−1 post-feeding in freshwater and seawater-acclimated fish, respectively. Based on predictions of gastric acid secreted during
digestion, we calculated net postprandial internal base gains (i.e., HCO3− secreted from gastric parietal cells into the blood) of 3.4 mmol kg−1 in seawater and 9.1 mmol kg−1 in freshwater-acclimated flounder. However, net fluxes of ammonia, titratable alkalinity, Na+ and Cl− indicated that branchial Cl−/HCO3− and Na+/H+ exchange played minimal roles in counteracting these predicted base gains and cannot explain the absence of alkaline tide.
Instead, intestinal Cl−/HCO3− exchange appears to be enhanced after feeding in both freshwater and seawater flounder. This implicates the intestine rather
than the gills as a potential route of postprandial base excretion in fish, to compensate for gastric acid secretion. 相似文献
7.
Taste buds and the peripheral nerves innervating them are two important components of the peripheral gustatory system. They
require appropriate connections for the taste system to function. Neurotrophic factors play crucial roles in the innervation
of peripheral sensory organs and tissues. Both brain-derived neurotrophic factor (BDNF) null-mutated and neurotrophin-4 (NT-4)
null-mutated mice exhibit peripheral gustatory deficits. BDNF and NT-4 bind to a common high affinity tyrosine kinase receptor,
TrkB (NTRK-2), and a common p75 neurotrophin receptor (NGFR). We are currently using a transgenic mouse model to study peripheral
taste system development and innervation in the absence of both TrkB ligands. We show that taste cell progenitors express
taste cell markers during early stages of taste bud development in both BDNF−/−xNT-4−/− and wild-type mice. At early embryonic stages, taste bud progenitors express Troma-1, Shh, and Sox2 in all mice. At later
stages, lack of innervation becomes a prominent feature in BDNF−/−xNT-4−/− mice leading to a decreasing number of fungiform papillae and morphologically degenerating taste cells. A total loss of vallate
taste cells also occurs in postnatal transgenic mice. Our data indicate an initial independence but a later permissive and
essential role for innervation in taste bud development and maintenance.
This work was supported by NIH-NIDCD R01-RDC007628. 相似文献
8.
CO2 and N-fertilization effects on fine-root length, production, and mortality: a 4-year ponderosa pine study 总被引:1,自引:0,他引:1
We conducted a 4-year study of juvenile Pinus ponderosa fine root (≤2 mm) responses to atmospheric CO2 and N-fertilization. Seedlings were grown in open-top chambers at three CO2 levels (ambient, ambient+175 μmol/mol, ambient+350 μmol/mol) and three N-fertilization levels (0, 10, 20 g m−2 year−1). Length and width of individual roots were measured from minirhizotron video images bimonthly over 4 years starting when the seedlings were 1.5 years old. Neither CO2 nor N-fertilization treatments affected the seasonal patterns of root production or mortality. Yearly values of fine-root length standing crop (m m−2), production (m m−2 year−1), and mortality (m m−2 year−1) were consistently higher in elevated CO2 treatments throughout the study, except for mortality in the first year; however, the only statistically significant CO2 effects were in the fine-root length standing crop (m m−2) in the second and third years, and production and mortality (m m−2 year−1) in the third year. Higher mortality (m m−2 year−1) in elevated CO2 was due to greater standing crop rather than shorter life span, as fine roots lived longer in elevated CO2. No significant N effects were noted for annual cumulative production, cumulative mortality, or mean standing crop. N availability did not significantly affect responses of fine-root standing crop, production, or mortality to elevated CO2. Multi-year studies at all life stages of trees are important to characterize belowground responses to factors such as atmospheric CO2 and N-fertilization. This study showed the potential for juvenile ponderosa pine to increase fine-root C pools and C fluxes through root mortality in response to elevated CO2. 相似文献
9.
Circadian rhythms in light-evoked responses of the fly's compound eye, and the effects of neuromodulators 5-HT and the peptide PDF 总被引:4,自引:0,他引:4
B. Chen I. A. Meinertzhagen S. R. Shaw 《Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology》1999,185(5):393-404
Two sets of wide-field neurons extend neurites into the fly's optic lamina, where monopolar cells receive photoreceptor input.
They exhibit immunoreactivity to antibodies raised against either 5-hydroxytryptamine or the crustacean peptide PDH, respectively.
Both are proposed whole-field neuromodulators of vision, apparently regulating a circadian rhythm of monopolar cell size.
Seeking functional correlates, we have re-examined the electroretinogram for circadian rhythmicity, and for responses to locally
injected 5-hydroxytryptamine and peptide. Long-term electroretinogram recordings from Calliphora entrained to a light/dark cycle and then transferred to constant darkness, uncovered a gradual, modest increase during the
subjective night in the electroretinogram's ON- and OFF-transients, from the lamina's monopolar cells. Five to twenty nl of
5-hydroxytryptamine (10−3 mol · 1−1) injected into the head haemolymph strongly enhanced the electroretinogram transients, an action reversed by 5-hydroxytryptamine
antagonists. Injected into the eye, 5-hydroxytryptamine (10−4 mol · 1−1) had the opposite effect; the rapid onset there suggests direct action, whilst the opposing effect from haemolymph injection
suggests a different receptor site. Pigment-dispersing hormone (2.2 × 10−5 mol · 1−1) injected into the haemolymph increased the electroretinogram transients along a biphasic course, with a slow partial recovery;
injected into the eye, it lacked effect.
Accepted: 30 May 1999 相似文献
10.
11.
To clarify the neuroprotective property of ceruloplasmin and the pathogenesis of aceruloplasminemia, we generated ceruloplasmin-deficient
(CP
−/−) mice on the C57BL/10 genetic background and further treated them with a mitochondrial complex I inhibitor, rotenone. There
was no iron accumulation in the brains of CP
−/− mice at least up to 60 weeks of age. Without rotenone treatment, CP
−/− mice showed slight motor dysfunction compared with CP
+/+ mice, but there were no detectable differences in the levels of oxidative stress markers between these two groups. A low
dose of rotenone did not affect the mitochondrial complex I activity in our mice, however, it caused a significant change
in motor behavior, neuropathology, or the levels of oxidative stress markers in CP
−/− mice, but not in CP
+/+ mice. Our data support that ceruloplasmin protects against rotenone-induced oxidative stress and neurotoxicity, probably
through its antioxidant properties independently of its function of iron metabolism. 相似文献
12.
Grzelak A Kruszewski M Macierzyńska E Piotrowski Ł Pułaski Ł Rychlik B Bartosz G 《Cellular & molecular biology letters》2009,14(1):23-34
The erythrocytes of 12-month old Sod1
−/−
mice showed an increased level of reactive oxygen species (ROS), as estimated by the degree of dihydroethidine and dihydrorhodamine
oxidation, and the increased level of Heinz bodies. No indices of severe oxidative stress were found in the red blood cells
and blood plasma of Sod1
−/−
mice as judged from the lack of significant changes in the levels of erythrocyte and plasma glutathione, plasma protein thiol
and carbonyl groups and thiobarbituric-acid reactive substances in the blood plasma. However, a decreased erythrocyte lifespan,
increased reticulocyte count and splenomegaly were noted, indicating the importance of superoxide dismutase for maintaining
erythrocyte viability. The levels of erythrocyte ROS and Heinz bodies and the reticulocyte count were indistinguishable in
Sod1
+/+
and Sod1
+/−
mice, suggesting that a superoxide dismutase activity decrease to half of its normal value may be sufficient to secure the
protective effects of the enzyme. 相似文献
13.
Vávrová J Sinkorová Z Rezáčová M Tichý A Filip S Mokrý J Lukášová E 《Radiation and environmental biophysics》2012,51(2):205-213
In the work presented here, changes in haematopoiesis of mice (B6129SF2/J) were studied 1 year after their whole-body exposure
to a dose of 7 Gy (72% of mice survived). The irradiated mice were compared with non-irradiated younger (4 months of age)
and older (16 months of age) mice. There was a significant increase in the relative abundance of primitive stem cells with
long-term capability of the haematopoiesis recovery lin−/Sca-1+/CD117+/CD34− in the bone marrow of mice aged 16 months (irradiated and non-irradiated) compared with those aged 4 months. In terms of
the ability to respond to further whole-body irradiation at a dose of 1 Gy, the presence of γH2A.X foci was studied in lin− bone marrow cells. There was a considerable number of persisting foci in lin− stem cells isolated from the bone marrow of the older irradiated mice. In the blood count from the peripheral blood of the
older mice (both non-irradiated and irradiated at 7 Gy), there was a significant increase in granulocytes. In the group exposed
to 7 Gy, the numbers of thrombocytes significantly increased, and on the contrary, the numbers of erythrocytes, the amount
of haemoglobin, and haematocrit significantly decreased. 相似文献
14.
We assessed the effect of salinity on plant growth and leaf expansion rates, as well as the leaf life span and the dynamics
of leaf production and mortality in seedlings of Avicennia germinans L. grown at 0, 170, 430, 680, and 940 mol m−3 NaCl. The relative growth rates (RGR) after 27 weeks reached a maximum (10.4 mg g−1 d−1) in 170 mol m−3 NaCl and decreased by 47 and 44% in plants grown at 680 and 940 mol m−3 NaCl. The relative leaf expansion rate (RLER) was maximal at 170 mol m−3 NaCl (120 cm m−2 d−1) and decreased by 57 and 52% in plants grown at 680 and 940 mol m−3 NaCl, respectively. In the same manner as RGR and RLER, the leaf production (P) and leaf death (D) decreased in 81 and 67% when salinity increased from 170 to 940 mol m−3 NaCl, respectively. Since the decrease in P with salinity was more pronounced than the decrease in D, the net accumulation of leaves per plant decreased with salinity. Additionally, an evident increase in annual mortality
rates (λ) and death probability was observed with salinity. Leaf half-life (t
0.5) was 425 days in plants grown at 0 mol m−3 NaCl, and decreased to 75 days at 940 mol m−3 NaCl. Thus, increasing salinity caused an increase in mortality rate whereas production of new leaves and leaf longevity
decreased and, finally, the leaf area was reduced. 相似文献
15.
R. Oelkrug G. Heldmaier C. W. Meyer 《Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology》2011,181(1):137-145
In eutherian mammals, uncoupling protein 1 (UCP1) mediated non-shivering thermogenesis from brown adipose tissue (BAT) provides
a mechanism through which arousal from torpor and hibernation is facilitated. In order to directly assess the magnitude by
which the presence or absence of UCP1 affects torpor patterns, rewarming and arousal rates within one species we compared
fasting induced torpor in wildtype (UCP1+/+) and UCP1-ablated mice (UCP−/−). Torpor was induced by depriving mice of food for up to 48 h and by a reduction of ambient temperature (T
a) from 30 to 18°C at four different time points after 18, 24, 30 and 36 h of food deprivation. In most cases, torpor bouts
occurred within 20 min after the switch in ambient temperature (30–18°C). Torpor bouts expressed during the light phase lasted
3–6 h while significantly longer bouts (up to 16 h) were observed when mice entered torpor during the dark phase. The degree
of hypometabolism (5–22 ml h−1) and hypothermia (19.5–26.7°C) was comparable in wildtype and UCP1-ablated mice, and both genotypes were able to regain normothermia.
In contrast to wildtype mice, UCP1-ablated mice did not display multiple torpor bouts per day and their peak rewarming rates
from torpor were reduced by 50% (UCP1+/+: 0.24 ± 0.08°C min−1; UCP1−/−: 0.12 ± 0.04°C min−1). UCP1-ablated mice therefore took significantly longer to rewarm from 25 to 32°C (39 vs. 70 min) and required 60% more energy
for this process. Our results demonstrate the energetic benefit of functional BAT for rapid arousal from torpor. They also
suggest that torpor entry and maintenance may be dependent on endogenous rhythms. 相似文献
16.
Here we show that low-dose cyclophosphamide (CY), that depends for its therapeutic effectiveness on the immunopotentiating
activity of the drug for T cell-mediated tumor-eradicating immunity, is curative for ~80% of wild-type (WT) mice bearing a
large s.c. MOPC-315 tumor, but only for ~10% of IFN-α/βR−/− mice bearing a large s.c. MOPC-315 tumor. Histopathological examination of the s.c. tumors of such mice on day 4 after the
chemotherapy revealed that the low dose of CY led to accumulation of T lymphocytes in both the WT and the IFN-α/βR−/− mice. However, in the CY treated tumor bearing WT mice the T lymphocytes were present throughout the tumor mass and in direct
contact with tumor cells, but in the CY treated tumor bearing IFN-α/βR−/− mice most of the T lymphocytes remained in blood vessels. In addition to being important for CY-induced transendothelial
migration of T lymphocytes into the tumor mass, we show here that signaling via the IFN-α/βR is also important for CY-induced
control of metastatic tumor progression in the spleen and liver of the tumor bearing mice. Finally, CY cured tumor bearing
WT mice were resistant to a subsequent challenge with MOPC-315 tumor cells, but the few CY cured tumor bearing IFN-α/βR−/− mice were not. Thus, signaling via the IFN-α/βR on host cells in MOPC-315 tumor bearers is important for CY-induced: (a)
transendothelial migration of T lymphocytes into the tumor mass and the eradication of the primary tumor, (b) control of metastatic
tumor progression, and (c) resistance to a subsequent tumor challenge.
This work was supported by Research Grant 03-19 from the American Cancer Society-Illinois Division. 相似文献
17.
Miao Yin Liang Zhang Xiao-ming Sun Liu-feng Mao Jie Pan 《Molecular biology reports》2010,37(4):2049-2054
To investigate the effect of apolipoprotein E (apoE) on cytokine expression profile of the liver of young mice, quantitative
RT-PCR (qRT-PCR) assay and cytokine antibody array for multiplex analysis of 62 cytokines have been used to analyze characteristics
of expression of cytokines in the liver of 6-week-old apoE-null (apoE−/−) mice. The levels of plasma cytokines were also analyzed. The mRNA level of IL-1β, IL-2, IL-6, ICAM-1, VCAM-1, MCP-1, NF-κB
(p65), IFN-γ and IκB-α were increased significantly in apoE−/− mice comparative to wild-type (WT) mice. IL-4, IL-10 and GM-CSF, however, were slightly decreased. Compared with WT, levels
of 21 cytokines altered twofold or more in apoE−/− mice, including 10 cytokines increased and 11 decreased. Expression patterns of IL-1β, IL-2, IL-4, IL-6, IL-10, GM-CSF, IFN-γ
and VCAM-1 showed identical trend between cytokine antibody array and qRT-PCR analysis. Moreover, levels of IL-1β, IFN-γ and
IL-6 in the plasma were elevated, while IL-4 was lightly decreased in apoE−/− mice compared to those in WT mice. These results implied that promotion of type I immune response in the liver of young apoE−/− mice due to alteration of these cytokines, and the phenotypes may be caused by the regulation of NF-κB. The inflammation
and lipid metabolism dysfunction in the liver cooperated in dysfunction of the liver in young apoE−/− mice. 相似文献
18.
Adler M Sweeney RE Hamilton TA Lockridge O Duysen EG Purcell AL Deshpande SS 《Cellular and molecular neurobiology》2011,31(6):909-920
Electrophysiological and ultrastructural studies were performed on phrenic nerve-hemidiaphragm preparations isolated from
wild-type and acetylcholinesterase (AChE) knockout (KO) mice to determine the compensatory mechanisms manifested by the neuromuscular
junction to excess acetylcholine (ACh). The diaphragm was selected since it is the primary muscle of respiration, and it must
adapt to allow for survival of the organism in the absence of AChE. Nerve-elicited muscle contractions, miniature endplate
potentials (MEPPs) and evoked endplate potentials (EPPs) were recorded by conventional electrophysiological techniques from
phrenic nerve-hemidiaphragm preparations isolated from 1.5- to 2-month-old wild-type (AChE+/+) or AChE KO (AChE−/−) mice. These recordings were chosen to provide a comprehensive assessment of functional alterations of the diaphragm muscle
resulting from the absence of AChE. Tension measurements from AChE−/− mice revealed that the amplitude of twitch tensions was potentiated, but tetanic tensions underwent a use-dependent decline
at frequencies below 70 Hz and above 100 Hz. MEPPs recorded from hemidiaphragms of AChE−/− mice showed a reduction in frequency and a prolongation in decay (37%) but no change in amplitude compared to values observed
in age-matched wild-type littermates. In contrast, MEPPs recorded from hemidiaphragms of wild-type mice that were exposed
for 30 min to the selective AChE inhibitor 5-bis(4-allyldimethyl-ammoniumphenyl)pentane-3-one (BW284C51) exhibited a pronounced
increase in amplitude (42%) and a more marked prolongation in decay (76%). The difference between MEPP amplitudes and decays
in AChE−/− hemidiaphragms and in wild-type hemidiaphragms treated with BW284C51 represents effective adaptation by the former to a high
ACh environment. Electron microscopic examination revealed that diaphragm muscles of AChE−/− mice had smaller nerve terminals and diminished pre- and post-synaptic surface contacts relative to neuromuscular junctions
of AChE+/+ mice. The morphological changes are suggested to account, in part, for the ability of muscle from AChE−/− mice to function in the complete absence of AChE. 相似文献
19.
N. Ishii M. Matsumura H. Kataoka H. Tanaka K. Araki 《Bioprocess and biosystems engineering》1995,13(3):119-123
Pervaporation using oleyl alcohol supported liquid membrane was successfully applied to diacetyl fermentation by immobilized
lactic acid bacteria. Diacetyl productivity was about 10 g·m−3·h−1, while productivity during batch fermentation was about 6 g·m−3·h−1. Diacetyl yield from consumed glucose was about 0.04 g·g−1 which was 4 times as large as that of batch fermentation. The pervaporation functioned favorably on actual fermentation broth.
The flux of the permeate and the diacetyl separation factor for the pervaporation were about 9 g·m−2·h−1 and 36, respectively, and these values were maintained at almost constant levels during fermentation. Diacetyl concentration
in the permeate was about 2 kg·m−3, which is sufficiently high for commercial use. 相似文献
20.
Stefano Carenini Dirk Montag Harold Cremer Melitta Schachner Rudolf Martini 《Cell and tissue research》1996,287(1):3-9
We have previously shown that mice deficient in the gene for the myelin-associated glycoprotein (MAG) develop normal myelin
in the peripheral nerves, but show axon and myelin degeneration at eight months of age, suggesting that MAG is involved in
the maintenance of axon-Schwann cell integrity. The search for molecules that might replace MAG during myelination revealed
an overexpression of the neural cell adhesion molecule (N-CAM) at those aspects where MAG is detectable in wild type mice.
To test whether N-CAM might compensate for MAG during myelination in MAG-deficient mice, double mutants deficient in both
MAG and N-CAM (MAG−/N-CAM−mice) were generated by cross-breeding the single mutants. Whereas alterations of myelin development were not detectable in
either of the single or double mutants, degeneration of myelin and axons occurred approximately 4 weeks earlier in MAG−/N-CAM−than in MAG−mutants. Furthermore, at 8 weeks of age, single fiber preparation and electron microscopy revealed that the number of profiles
indicative of degeneration was substantially increased in MAG−/N-CAM−mutants when compared to MAG−mice. These data suggest that in MAG-deficient mice N-CAM does not compensate for MAG in myelin formation but partially substitutes
for it in the maintenance of axon-myelin integrity.
Received: 20 May 1996 / Accepted: 19 July 1996 相似文献