共查询到20条相似文献,搜索用时 31 毫秒
1.
Ting-ting Liu Jie Shi David H. Epstein Yan-ping Bao Lin Lu 《Cellular and molecular neurobiology》2009,29(4):449-454
This review extends a prior meta-analysis of acupuncture’s utility for treating opioid detoxification, addressing the efficacy
of acupuncture when combined with allopathic therapies. Both English and Chinese databases were searched for randomized trials
comparing acupuncture combined with opioid agonist treatment versus opioid agonists alone for treating symptoms of opioid
withdrawal. The methodological quality of each study was assessed with Jadad’s scale (1–2 = low; 3–5 = high). Meta-analysis
was performed with fixed- or random-effect models in RevMan software; the outcome measures assessed were withdrawal-symptoms
score, relapse rate, side effects, and medication dosage. Withdrawal-symptom scores were lower in combined treatment trials
than in agonist-alone trials on withdrawal days 1, 7, 9, and 10. Combined treatment also produced lower reported rates of
side effects and appeared to lower the required dose of opioid agonist. There was no significant difference on relapse rate
after 6 months. This meta-analysis suggests that acupuncture combined with opioid agonists can effectively be used to manage
the withdrawal symptoms. One limitation of this meta-analysis is the poor quality of the methodology of some included trials.
High-quality studies are needed to confirm findings regarding the side effects and medication dosage. 相似文献
2.
M. V. Konakov L. P. Dolgacheva E. A. Turovsky G. E. Bronnikov 《Biochemistry (Moscow) Supplemental Series A: Membrane and Cell Biology》2010,4(1):64-69
Brown adipose tissue of small animals in the cold is able to increase several fold its mass and ability for non-shivering
thermogenesis. Adrenergic agonists play a crucial role in the stimulation of the tissue hyperplasia and thermoregulation.
In this work, a comparative study of the Ca2+ signaling in mouse and ground squirrel brown preadipocytes was carried out. The goal of this study was to elucidate what
features of the Ca2+ signaling in ground squirrel preadipocytes allow the hibernators to control brown fat hyperplasia in the absence of cold
stress. This knowledge would enable us to find ways to control human body mass and to treat diabetes mellitus type two. Low
concentrations (0.3–3 μM for mouse cells and 1–10 μM for ground squirrel cells) of the selective α1- and β-adrenergic agonists cirazoline and isoproterenol, respectively, induced slow Ca2+ responses with linear kinetics in brown preadipocytes of both species. High concentrations of the agonists (10–500 μM) caused
Ca2+ responses with exponential kinetics in ground squirrel brown preadipocytes and suppressed the responses in mouse preadipocytes.
Dose-response curves for the agonists were bell-shaped for both mouse and ground squirrel preadipocytes. It should be noted
that in preadipocytes of both species β-adrenergic agonist induced stronger responses than α1-adrenergic agonist did. On the other hand, the responses evoked in ground squirrel brown preadipocytes by both agonists were
two orders of magnitude stronger than the responses in mouse preadipocytes. Treatment of the cells with forskolin demonstrated
that brown preadipocytes of a ground squirrel had a strong positive feedback in Ca2+ signaling, whereas mouse preadipocytes had a negative feedback. The difference found in the preadipocyte Ca2+ signaling may explain the different strategies employed in the two species for the regulation of their body fat mass and
survival in the cold. 相似文献
3.
Jianxin Cheng Guixia Liu Jing Zhang Zhejun Xu Yun Tang 《Journal of molecular modeling》2011,17(3):477-493
To probe the selective mechanism of agonists binding to three opioid receptor subtypes, ligand-based and receptor-based methods
were implemented together and subtype characteristics of opioid agonists were clearly described. Three pharmacophore models
of opioid agonists were generated by the Catalyst/HypoGen program. The best pharmacophore models for μ, δ and κ agonists contained
four, five and five features, respectively. Meanwhile, the three-dimensional structures of three receptor subtypes were modeled
on the basis of the crystal structure of β2-adrenergic receptor, and molecular docking was conducted further. According to
these pharmacophore models and docking results, the similarities and differences among agonists of three subtypes were identified.
μ or δ agonists, for example, could form one hydrogen bond separately with Tyr129 and Tyr150 at TMIII, whereas κ ones formed
a π-π interaction in that place. These findings may be crucial for the development of novel selective analgesic drugs. 相似文献
4.
Published data on the association between β1-adrenergic receptor gene polymorphisms and idiopathic dilated cardiomyopathy (IDCM) risk are inconclusive. To derive a more
precise estimation of the relationship, a meta-analysis was performed. A total of 12 case–control studies including 2642 cases
and 3136 controls provided data on the association between β1-adrenergic receptor gene polymorphisms and susceptibility to IDCM. Overall, no significantly elevated risk was associated
with Arg389Gly polymorphisms for all genetic models. In the subgroup analysis by ethnicity, no statistically increased risk
was found for Gly389Gly versus Arg389Arg (OR 0.73; 95% CI 0.54–0.99; P
h = 0.35) and Gly389Gly versus Arg389Arg + Arg389Gly (OR 0.75; 95% CI 0.55–1.01; P
h = 0.52) among Europeans. Meanwhile, significantly increased risk was found among Asians based on the relatively small sample
size. Further, significantly elevated IDCM risk was associated with Ser49Gly polymorphisms for all genetic models. When stratified
by ethnicity, statistical association was found among Asians for Gly49Gly versus Ser49Ser (OR 4.56; 95% CI 1.36–15.23; P
h = 0.10) and Gly49Gly versus Ser49Ser + Ser49Gly (OR 4.49; 95% CI 1.33–15.15; P
h = 0.12), but not among Europeans. In summary, this meta-analysis suggests that no statistically increased risk was found
between β1-adrenergic receptor gene polymorphisms and susceptibility to IDCM among Europeans. 相似文献
5.
Ivar Aursnes Jan-Bjørn Osnes Ingunn Fride Tvete Jørund Gåsemyr Bent Natvig 《BMC clinical pharmacology》2007,7(1):4
Background
A recent meta-analysis of drug effects in patients with hypertension claims that all β-adrenergic blockers are equally effective but less so than other antihypertensive drugs. Published comparisons of the β-adrenergic blocker atenolol and non-atenolol β-adrenergic blockers indicate different effects on death rates, arrhythmias, peripheral vascular resistance and prognosis post myocardial infarction, all in disfavour of atenolol. In keeping with these findings, the data presented in the meta-analysis indicate that atenolol is less effective than the non-atenolol β-adrenergic blockers both when compared with placebo and with other antihypertensive drugs. These findings were not, however, statistically significant. 相似文献6.
The activity of dehydroleucodine, a sesquiterpene lactone obtained from Artemisia douglasiana, was studied in mice small intestinal
transit. Its mechanism was evaluated in the presence of several adrenergic and cholinergic antagonist drugs and one opioid
antagonist. Docking of dehydroleucodine into the homology model of the α2-adrenergic receptor allowed us to analyze the structural
basis of their interactions. The experiments showed that dehydroleucodine delayed intestinal transit. The docking of dehydroleucodine
showed a unique binding site, equivalent to the binding site of carozolol in the β-adrenergic receptor. The results suggested
that dehydroleucodine produced an inhibitory effect on intestinal transit. Its action could be mediated, at least in part,
through the α2-adrenergic receptor. 相似文献
7.
Mustafa Cemek Mehmet Emin Büyükokuroğlu Ömer Hazman Muhsin Konuk Sait Bulut Yavuz Osman Birdane 《Biological trace element research》2011,142(1):55-66
The therapeutic effects of melatonin or vitamin E plus Se (vE + Se) on the restrain of the heroin withdrawal-induced oxidative
stress were studied. For this, rats were divided into ten groups. The rats were injected by fixed or variable doses of heroin
for 16 consecutive days, and naloxone was given 1 h after the last heroin injection. One hour after naloxone administration,
some groups were treated with melatonin or vE + Se. After 1 h this, blood samples were taken, and the levels of malondialdehyde
(MDA) and reduced glutathione (GSH) in whole blood, ascorbic acid, α-tocopherol, retinol, β-carotene, nitrite, nitrate, and
ceruloplasmin levels in the serum were measured. Our findings showed that, naloxone administration precipitated the heroin
withdrawal. This also increased the level of MDA and decreased the levels of GSH in blood. Melatonin or vE + Se administration
prevented the rise in MDA levels and increased the GSH levels. On the other hand, there were some significant differences
between α-tocopherol, retinol, β-carotene, nitrite, nitrate, and ceruloplasmin levels of experimental groups. Results of present
study showed that heroin withdrawal increased the lipid peroxidation and depressed endogenous antioxidative systems. Additionally,
melatonin or vE + Se administrations prevented lipid peroxidation and augmented endogenous antioxidant defense systems. 相似文献
8.
The effects of cholinergic and α-adrenergic stimulation (in vivo and in vitro) on the monovalent ion content of rat submandibular
gland acinar cells were evaluated at the subcellular level by X-ray microanalysis. Fragments of glands or enzymatically dispersed
acini were slam-frozen and cut into ultrathin cryosections. Spectra were collected from secretory granules, nucleus, the basal
cytoplasm containing endoplasmic reticulum and the apical cytoplasm identified between secretory granules. No significant
changes in Na and Cl content were observed after the isolation of acini, but the K concentration decreased compared with cells
from in situ glands. The Cl and K content in all four compartments studied decreased significantly after cholinergic stimulation
both in vivo and in vitro but in a more restricted fashion after α-adrenergic stimulation. Our findings indicate that: (1)
the physiological mechanisms regulating the monovalent ion composition of submandibular cells are relatively well preserved
in isolated acinar cells; (2) the results from in vivo experiments are in good agreement with those from in vitro experiments;
and (3) the effects of cholinergic and α-adrenergic stimulation on the K+ and Cl–efflux at the subcellular level are similar but the response is generally less with α-adrenergic stimulation.
Accepted: 24 April 1997 相似文献
9.
The aim of this study was to explore whether the cytotoxic T lymphocyte associated antigen-4 (CTLA-4) or tumor necrosis factor-α
(TNF-α) polymorphisms contribute to anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) susceptibility.
The authors conducted a meta-analysis on associations between polymorphisms of the 3′ untranslated region (UTR) microsatellite
at exon 3, exon 4 CT60 (A/G), exon 1 +49 (A/G), and promoter -318 (C/T) of CTLA-4, and TNF-α promoter-308 (A/G) and AAV susceptibility
as determined using; (1) allelic contrast and (2) homozygote contrast, (3) recessive, and (4) dominant models. A total of
11 comparisons were considered in this meta-analysis. These studies encompassed 7 CTLA-4 studies and 4 TNF-α studies in 10
European populations and 1 Asian population. The (AT)n repeat polymorphisms of CTLA-4 were found to be significantly associated with AAV in European populations (OR of 86 vs. xx
allele = 0.402, 95% CI = 0.184–0.875, P = 0.022). The one study conducted on this polymorphism in Asians showed no significant association with AAV. Meta-analysis
of the 86/86 (recessive effect), 86/86 and 86/xx (dominant effect), and 86/86 vs. xx/xx (homozygote contrast) of the (AT)n repeat revealed a significant association with AAV in Europeans. Both the CTLA-4 CT60 and +49 polymorphisms were found to be significantly associated with AAV in European populations, and allele and genotype-based
analyses showed a significant association between the CTLA-4 CT60 and +49 polymorphisms with AAV in Europeans (OR of the A allele of CT60 = 0.769, 95% CI = 0.619–0.017, P = 0.035; OR of the T allele of +49 = 1.382, 95% CI = 1.147–1.664, P = 0.001, respectively). Meta-analysis of the CTLA-4 -318 polymorphism failed to identify any association with AAV. Furthermore, meta-analysis of the AA genotype, the AA and
AG genotypes, and the A allele of TNF-α failed to reveal any association with Wegener’s granulomatosis (WG). This meta-analysis
demonstrates that the CTLA-4 polymorphisms confer susceptibility to AAV in Europeans. In contrast, no association was found
between the TNF-α-308 polymorphism and susceptibility to WG in Europeans. 相似文献
10.
Xavier Busquets Pablo V. Escriba Magdalena Sastre Jesús A. García-Sevilla 《Journal of neurochemistry》1995,64(1):247-252
Abstract: The biochemical status of human brain protein kinase C (PKC)-αβ during opiate dependence was studied by means of immunoblotting techniques in postmortem brain of heroin addicts who had died by opiate overdose. In the frontal cortex, a marked decrease (53%, p < 0.05) in the immunoreactivity of PKC-αβ was found in heroin addicts compared with matched controls. The loss of PKC-αβ in the brain of human addicts paralleled that observed in the frontal cortex of rats after chronic treatment with morphine (10–100 mg/kg i.p. for 5 days) (PKC-αβ decreased by 34%, p < 0.05). Chronic treatment with naloxone (1 mg/kg i.p. every 12 h for 5 days) did not alter PKC-αβ immunoreactivity in the rat brain. However, in morphine-dependent rats, naloxone-precipitated withdrawal induced a rapid and strong behavioral reaction with a concomitant up-regulation of PKC-αβ immunoreactivity to control values. These results indicated that the decrease of brain PKC-αβ induced by heroin/morphine is a μ-opioid receptor-mediated effect. The chronic administration of opiates has been associated with a marked sensitization of the adenylyl cyclase/cyclic AMP system, although this phenomenon is not exclusive of the opioid system but the general cellular adaptation to chronic inhibition of adenylyl cyclase. In this context, chronic treatment of rats with other inhibitory agonists (e.g., clonidine, 1 mg/kg i.p. every 12 h for 14 days) acting through receptors (e.g., α2 -adrenoceptors) also coupled to adenylyl cyclase did not alter brain PKC-αβ immunoreactivity. Together these findings suggest that the brain PKC system might play a major role in opiate addiction. 相似文献
11.
Cyclin D1 represents a key molecule in the regulation of cell cycle. CCND1 G870A (rs603965) polymorphism has drawn considerable
attention as the A allele may generate a variant splice product with possible oncogenic actions. A meta-analysis examining
the association between CCND1 G870A polymorphism and breast cancer risk was performed. Separate analyses on Caucasian and
Chinese populations were also implemented. Eligible articles were identified for the period up to July 2010. Pooled odds ratios
(OR) were appropriately derived from fixed-effects or random-effects models. Sensitivity analysis excluding studies whose
genotype frequencies in controls significantly deviated from Hardy–Weinberg Equilibrium (HWE) was performed. Nine case–control
studies on Caucasians (7,304 cases and 8,149 controls) and four case–control studies on Chinese (2,607 cases and 3,022 controls)
were eligible. At the overall analysis the A allele seemed to be associated with elevated breast cancer risk; the effect seemed
to be confined to homozygous carriers (pooled OR = 1.091, 95% CI: 1.008–1.179, P = 0.030, fixed effects) as heterozygous carriers did not exhibit significantly elevated breast cancer risk. No statistically
significant associations were demonstrated in Caucasians. On the other hand, Chinese AA carriers exhibited marginally elevated
breast cancer risk (pooled OR = 1.144, 95% CI: 0.984–1.329, P = 0.080, fixed effects). Nevertheless, the controls in two out of the four Chinese studies deviated from HWE. In conclusion,
this meta-analysis suggests that the A allele of the CCND1 G870A polymorphism may confer additional breast cancer risk when
it comes to homozygosity and Chinese populations. The need for additional, methodologically sound studies on Chinese populations
seems warranted. 相似文献
12.
The published data on the association between xeroderma pigmentosum group D (XPD) Lys751Gln polymorphism and esophageal cancer
(EC) remained controversial. The present meta-analysis of literatures was performed to derive a more precise estimation of
the relationship. A comprehensive literature search was conducted to identify all case–control studies of Lys751Gln polymorphism
and risk for two main types of EC: esophageal adenocarcinoma (EADC) and esophageal squamous cell carcinoma (ESCC). A total
of 12 studies were identified to the meta-analysis, including 2,575 cases (1,294 ESCC and 1,281 EADC) and 4,951 controls (1,891
ESCC and 3,060 EADC). Random-effects or fix-effects model was used according to between-study heterogeneity. The odds ratio
(OR) for the variant homozygous genotype Gln/Gln of the Lys751Gln polymorphism, compared with the wild type homozygote Lys/Lys,
was 1.26, with 95% confidence interval (95% CI) 1.02–1.56, for EADC risk without between-study heterogeneity. When stratified
by ethnicity, statistically significantly elevated risk was found among Chinese (Gln/Gln vs. Lys/Lys: OR 2.45, 95% CI = 1.10–5.44).
However, no significant associations were found between XPD Lys751Gln polymorphism and EC risk when all studies pooled into
the meta-analysis (Lys/Gln vs. Lys/Lys: OR 1.07, 95% CI = 0.88–1.28; Gln/Gln vs.us Lys/Lys: OR 1.25, 95% CI = 0.92–1.71; dominant
model: OR 1.09, 95% CI = 0.90–1.33). In conclusion, this meta-analysis suggests that the Lys751Gln genetic polymorphism may
be a potential biomarker of EC susceptibility in Chinese populations. And a study with the larger sample size is needed to
further evaluate gene–environment interaction on XPD Lys751Gln polymorphism and EC risk. 相似文献
13.
Görel Nyman Stina Marntell Anna Edner Pia Funkquist Karin Morgan Göran Hedenstierna 《Acta veterinaria Scandinavica》2009,51(1):22
Background
Sedation with α2-agonists in the horse is reported to be accompanied by impairment of arterial oxygenation. The present study was undertaken to investigate pulmonary gas exchange using the Multiple Inert Gas Elimination Technique (MIGET), during sedation with the α2-agonist detomidine alone and in combination with the opioid butorphanol. 相似文献14.
The aim of this study was to evaluate the association between various cytokine gene polymorphisms and lung cancer (LC) susceptibility.
We searched Pubmed, Elsevier Science Direct, China National Knowledge Infrastructure database, Chinese Biomedical database,
Google scholar. Totally, 20 studies involving 6,467 cases and 8,320 controls were included in the meta-analysis. The effects
of eight polymorphisms, i.e. TNF-α 308G/A, IL-6 174G/C, IL-1β 31T/C, IL-1β 511C/T, COX-2 8473T/C, IL-10 1082G/A, IL-10 819C/T,
and IL-10 592C/A were evaluated. The combined odds ratio (OR) with 95% confidence interval (95% CI) was calculated to estimate
the strength of the association in a fixed or random effect model. Heterogeneity and publication bias were also assessed.
We found a significant association between IL-10 polymorphism and LC. For IL-10 1082G/A, the overall ORs (95% CI) of the G
versus A, GG versus AA, and GG/GA versus AA were 2.35 (1.16–4.76), 2.07 (1.16–3.70) and 3.17 (1.31–7.68), respectively. For
IL-10 819C/T, the pooled ORs (95% CI) of the C versus T and CC versus TT were 1.27 (1.01–1.58) and 2.27 (1.32–3.89). For IL-10
592C/A, the comparison of subjects in the CC or CC/CA genotype versus AA homozygotes showed significant results (OR = 2.00,
95% CI: 1.24–3.23; OR = 1.80, 95% CI: 1.28–2.54). But, other gene polymorphisms did not reach statistical associations. IL-10
1082G/A, 819C/T and 592C/A polymorphisms might be risk factors for LC. TNF-α 308G/A, IL-6 174G/C, IL-1β 31T/C, IL-1β 511C/T,
COX-2 8473T/C polymorphisms were not detected to be related to the risk for LC. Due to the limitation of the number of the
studies, we should take the conclusion with caution. While, further studies are necessary for more precise association. 相似文献
15.
Posokhova EN Khoshchenko OM Chasovskikh MI Pivovarova EN Dushkin MI 《Biochemistry. Biokhimii?a》2008,73(3):296-304
The effects of peroxisome proliferator activated receptors α and γ (PPAR-α and PPAR-γ) and retinoid X receptor (RXR) agonists
upon synthesis and accumulation of lipids in murine C57B1 macrophages during inflammation induced by injection of zymosan
and Escherichia coli lipopolysaccharide (LPS) have been studied. It is significant that intraperitoneal injection of zymosan (50 mg/kg) or LPS
(0.1 mg/kg) in mice led to a dramatic increase of [14C]oleate incorporation into cholesteryl esters and triglycerides and [14C]acetate incorporation into cholesterol and fatty acids in peritoneal macrophages. Lipid synthesis reached its maximum rate
18–24 h after injection and was decreased 5–7 days later to control level after LPS injection or was still heightened after
zymosan injection. In macrophages obtained in acute phase of inflammation (24 h), degradation of 125I-labeled native low density lipoprotein (NLDL) was 4-fold increased and degradation of 125I-labeled acetylated LDL (AcLDL) was 2–3-fold decreased. Addition of NLDL (50 μg/ml) or AcLDL (25 μg/ml) into the incubation
medium of activated macrophages induced 9–14-and 1.25-fold increase of cholesteryl ester synthesis, respectively, compared
with control. Addition of NLDL and AcLDL into the incubation medium completely inhibited cholesterol synthesis in control
macrophages but had only slightly effect on cholesterol synthesis in activated macrophages. Injection of RXR, PPAR-α, or PPAR-γ
agonists—9-cis-retinoic acid (5 mg/kg), bezafibrate (10 mg/kg), or rosiglitazone (10 mg/kg), respectively—30 min before zymosan or LPS injection
led to significant decrease of lipid synthesis. Ten hour preincubation of activated in vivo macrophages with the abovementioned agonists (5 μM) decreased cholesteryl ester synthesis induced by NLDL and AcLDL addition
into the cell cultivation medium. The data suggest that RXR, PPAR-α, or PPAR-γ agonists inhibited lipid synthesis and induction
of cholesteryl ester synthesis in inflammatory macrophages caused by capture of native or modified LDL.
Published in Russian in Biokhimiya, 2008, Vol. 73, No. 3, pp. 364–374. 相似文献
16.
Functional activation of α2A adrenergic receptors in the crude membranes from rat frontal cortex was studied by a [35S]-guanosine 5′-O-(γ-thiotriphosphate) ([35S]GTPγS) binding assay. α2A agonists UK14304 and guanfacine decreased the ability of GDP to compete with [35S]GTPγS binding to the membranes and 0.1 mM GDP was found to be optimal for the following functional experiments. However,
even after careful optimization of experimental conditions the specificity of ligands for rat α2 adrenoceptors were not sufficient, as agonists as well as antagonists became activators of other signal transduction systems
before achieving their maximal effect in the α2A-adrenergic system. Only using compromising concentration of agonist (up to 1 μM UK14304) and antagonist (up to 1 μM RS79948)
to inhibit agonist’s effect, allowed us to filtrate out α2A specific effect for characterization of signal transduction in rat frontal cortex membranes for the comparison efficacies
of this system for different animals from behavioral experiments. 相似文献
17.
Benjamins JA Nedelkoska L Lisak RP Hannigan JH Sokol RJ 《Neurochemical research》2011,36(9):1677-1686
To characterize immunomodulatory mechanisms that affect oligodendroglia (OL) and white matter following ethanol exposure during
early CNS development, we investigated the direct effects of ethanol and cytokines on glia. Mixed glial cultures from newborn
rat brain were exposed to 6.5–130 mM ethanol for 1–3 days. OL were sensitive to ethanol, with death ranging from 32 to 88%
with increasing time and ethanol concentrations. Little cell death occurred in astroglia or microglia. Mixtures of cytokines
representative of those produced by pro-inflammatory Th1 and monocyte/macrophage (M/M) cells as well as those produced by
anti-inflammatory Th2 cells were all protective. Three of the cytokines in the Th1 mixture, IL-2, TNF-α and IFN-γ, were protective
individually, although no single cytokine was as effective as the mixture. The protective effects of the Th1 mixture and of
IL-2 were reversed by inhibition of both MAP kinase and PI-3 kinase signaling pathways. We conclude that cytokines can act
either directly on OL or indirectly through effects on astroglia or microglia to protect OL from ethanol toxicity. 相似文献
18.
Ruisong Yu Shijuan Dong Yumin Zhu Hu Jin Mingjie Gao Zuoying Duan Zhiyong Zheng Zhongping Shi Zhen Li 《Bioprocess and biosystems engineering》2010,33(4):473-483
Efficient porcine interferon-α (pIFN-α) expression in high density recombinant Pichia pastoris cultivation was achieved in a 5 l bench-scaled bioreactor. The results indicated that a high and stable oxygen uptake rate
(OUR) during induction phase was closely related with pIFN-α production efficiency. The multi-variables clustering and analysis
results showed that the achievement of a high and stable OUR relied on a higher glycerol consumption rate during fed-batch
culture phase and a moderate methanol level (around 10 g/l) during induction phase. In the high and stable OUR environments
(200–300 mmol/l/h), the highest pIFN-α antiviral activity could reach a level of 6.7 × 106 IU/ml, which was more than 10–300-folds higher than those obtained at lower OUR (80–200 mmol/l/h) using the same bioreactor
and those obtained in shaking flasks. Clustering and analysis of the specific growth and glycerol consumption rates data during
culture phase could detect the ill fermentation state at early stage, potentially provided a simple and effective fault alarming/diagnosis
method for the achievement of stable pIFN-α production. 相似文献
19.
Tumor necrosis factor-alpha (TNF-α) has been regarded as a candidate gene for Crohn’s disease (CD) based on its inflammatory function in immune reaction and
the clinical effectiveness of anti-TNF-α therapy. However, studies to date have reported inconsistent findings for the association
between TNF-α and CD. The PubMed, EMBASE, and Medline databases were systematically reviewed from all English language publications
up to April, 2011. A total of twenty-nine studies concerning the association between CD and the TNF-α promoter polymorphisms of −308G/A, −857C/T and −238G/A were identified, among of them only twenty-three studies match the
inclusion criteria (including 3,843 cases and 6,260 controls) and were selected for the statistical test. We found that neither
the G allele of −308G/A (OR 1.02, 95% CI 0.87–1.19, P = 0.84), C allele of −857C/T (OR 0.97, 95% CI 0.86–1.09, P = 0.57) and G allele of −238G/A (OR 0.91, 95% CI 0.70–1.18, P = 0.48), and nor their GG (OR 1.05, 95% CI 0.88–1.25, P = 0.59), CC (OR 0.98, 95% CI 0.86–1.12, P = 0.76) and GG (OR 0.92, 95% CI 0.70–1.21, P = 0.55) genotypes were associated with CD susceptibility, respectively. Our meta-analysis demonstrates that three promoter
polymorphisms of TNF-α above may not confer susceptibility to CD. 相似文献
20.
The effects of acute and chronic morphine treatments on the expression of Ca2+/calmodulin dependent protein kinase II (CaMK II) gene in rat brain were investigated using in situ hybridization histochemistry.
Our data showed that repeated, but not single morphine administration, resulted in significant up-regulation of the α-CaMK
II gene expression in hippocampus and frontal cortex. We further studied the time courses of α-CaMK II gene expression in
response to repeated morphine administration. After 3 days of consecutive morphine injections, the α-CaMK II mRNA levels exhibited
a trend of up-regulation, and after 6 days of consecutive morphine injections it increased over 50–60% as compared with the
control group. The α-CaMK II mRNA levels remained high 24 h after the cessation of chronic morphine treatment and returned
to the control level 72 h later. However, changes of α-CaMK II gene levels mentioned above were not detected in amygdala or
piriform cortex. Taken together, our data demonstrate that chronic morphine treatment region-specific up-regulates the levels
of the α-CaMK II gene expression in hippocampus and frontal cortex.
Yuejun Chen, Yan Jiang, Wen Yue contributed equally to this work.
Special issue in honor of Dr. Ji-Sheng Han. 相似文献