Biomedical subjects

Mei Xu

Publications and source records attributed to Mei Xu.

At least 19 recordsLinked to original sources

PubMed2026

Branching plasticity and candidate gene-hormone networks associated with shade responses in soybean under relay strip intercropping.

BACKGROUND: Branching is a key determinant of high-yield plant architecture in soybean, particularly in maize- soybean relay strip intercropping where plants experience an "initially shaded-then fully illuminated" light regime. However, the genetic regulation of branching responses to shading remains poorly understood. METHODS: We evaluated 11 branching-related traits across 202 soybean accessions grown under monoculture (SS) and relay strip intercropping (RI). Branch number (BN), branching incidence (BI), and total branch length (TBL) were assessed together with stress tolerance indices (STI) and relative distance plasticity index (RDPI). Genome-wide association studies (GWAS) using mixed linear model (MLM) and three-variance-component MLM (3VmrMLM) were combined with haplotype and protein structural analyses to refine candidate genes. RESULTS: Based on Pearson correlation analysis of all 11 traits, BN, BI, and TBL measured before maize harvest showed the strongest and most consistent associations with branch seed weight within the corresponding cropping system (BSW_SS under SS and BSW_RI under RI), whereas other traits showed weaker or environment-dependent associations. Higher STI values calculated from these traits during the co-growth phase were negatively associated with BSW_RI, suggesting weaker compensatory recovery after light restoration in genotypes with more stable early branching patterns between SS and RI. In contrast, mediation analysis indicated that RDPI was positively associated with BSW_RI mainly through improved mature branching architecture (MB_index), which accounted for approximately 70% of the total positive effect. GWAS identified 57 and 74 significant QTNs using MLM and 3VmrMLM, respectively, and LD-window genes were filtered for exonic nonsynonymous or premature stop-codon variants, yielding 883 genes with putative functional variants. Two high-confidence genes emerged: Glyma.02G058600 (PP2C55), exhibiting shading-specific haplotype effects likely linked to GA-mediated branch-stem balance, and Glyma.02G059900 (DA1-related protein), showing stable effects across environments and implicated in ABA-mediated suppression of axillary meristems. CONCLUSIONS: These results provide insight into the genetic and physiological basis of soybean branching responses under relay strip intercropping, clarify that branching plasticity and relative shade tolerance represent distinct response dimensions in this system, and identify putative loci that may be useful for breeding soybean cultivars with improved shade adaptation and yield stability.

Glycine max↗

PubMed2025

Chromosome-level assembly and annotation of the yellow-shelled fish (Barbodes Wynaadensis).

Barbodes wynaadensis, a unique cyprinid species native to Yunnan Province in China, stands out as an allotetraploid (AABB) fish with a complex evolutionary history. Leveraging a multi-platform sequencing strategy combining MGI short-read, PacBio long-read, and Hi-C scaffolding technologies, we assembled the first chromosome-level genome for B. wynaadensis. The final assembled genome spans 1.76 Gb in length with a contig N50 of 33.53 Mb, demonstrating high assembly continuity. Hi-C scaffolding enabled the reconstruction of 50 pseudochromosomes, representing 99.94% of the total genome assembly. Genome annotation identified 46,121 protein-coding genes, with a functional annotation rate of 99.76%. Repetitive elements constituted 48.26% of the genomic sequences, including lineage-specific expansions of DNA transposons (29.26%) and LTRs (6.36%). This high-quality assembly resolves challenges in polyploid genome reconstruction and provides a critical resource for investigating Cyprinidae evolution, particularly subgenome divergence and adaptation. The dataset also enables practical applications, such as molecular marker development for population monitoring, supporting conservation efforts for this threatened endemic species amid habitat degradation in the Nujiang River basin.

Animals↗

PubMed2006

Bone morphogenetic protein and retinoic acid-inducible neural specific protein-3 is expressed in gonadotrope cell pituitary adenomas and induces proliferation, migration, and invasion.

Pituitary tumors are common intracranial neoplasms that often result in endocrine dysfunction due to hormone overproduction or deficiencies from mass effects. Gonadotrope cell or gonadotropinomas are tumors that produce LH and/or FSH and represent 40% of macroadenomas. Little is known about their underlying pathogenic mechanisms. We compared expression profiles of 10 gonadotropinomas with nine normal pituitaries by cDNA array and identified bone morphogenetic protein- and retinoic acid-inducible neural-specific protein-3 (BRINP3) as overexpressed in tumors, compared with normals. BRINP3 is a novel, normally brain restricted protein of unknown function. BRINP3 mRNA was expressed selectively in gonadotropinomas. Subcellular localization studies showed that BRINP3 was targeted to the mitochondria, but BRINP3 overexpression was unable to protect pituitary cells against programmed cell death induced by growth factor withdrawal. However, BRINP3 overexpression in pituitary gonadotrope cells promoted proliferation, migration, and invasion. A BRINP3 antibody was raised that demonstrated clustered expression of BRINP3 protein in gonadotropinomas and not in normal human pituitary samples. Thus, BRINP3 is a mitochondrially localized protein that is selectively up-regulated in human gonadotropinomas. Its actions to increase proliferation, migration, and invasion suggest it may play an important role in pituitary tumorigenesis.

Adenoma↗

PubMed2006

NMDA receptor-mediated activation of medullary pro-nociceptive neurons is required for secondary thermal hyperalgesia.

There is now direct evidence that a class of neurons in the rostral ventromedial medulla (RVM) exerts a net facilitatory influence on spinal nociception. The present experiments were designed to test whether activation of these neurons, referred to as "on-cells", is required as part of a positive feedback loop leading to secondary hyperalgesia in acute inflammation produced by topical application of mustard oil. Activity of a characterized RVM neuron and paw withdrawals to heat (plantar surface) were recorded in barbiturate-anesthetized rats. Following three baseline trials, mustard oil was applied to the skin above the knee. Cell activity and paw withdrawal latencies were monitored for an additional 45min. Application of mustard oil produced an increase in on-cell discharge that was associated with a substantial decrease in withdrawal latency of the ipsilateral paw. Blocking on-cell activation using local infusion of the NMDA-receptor antagonist AP5 into the RVM prevented hyperalgesia. Secondary thermal hyperalgesia following mustard oil was also associated with a significant decrease in the firing of "off-cells", a cell population thought to exert a net inhibitory influence on nociception. Depression of off-cell firing was unaffected by AP5 microinjection. The firing of "neutral cells", which have no documented role in nociceptive modulation, was unchanged following mustard oil and also unaffected by AP5 infusion in the RVM. Brainstem descending controls are receiving increasing attention in efforts to understand hyperalgesia and persistent pain states. The present experiments demonstrate that a novel, NMDA-mediated activation of on-cells is required for secondary thermal hyperalgesia in acute inflammation.

Action Potentials↗

PubMed2006

Extracellular signal-regulated kinase (ERK) 5 is necessary and sufficient to specify cortical neuronal fate.

Multipotent cortical progenitor cells differentiate into neurons and glial cells during development; however, mechanisms governing the specification of progenitors to a neuronal fate are not well understood. Although both extrinsic and intrinsic factors regulate this process, little is known about kinase signaling mechanisms that direct neuronal fate. Here, we report that extracellular signal-regulated kinase (ERK) 5 is expressed and active in proliferating cortical progenitors. Lentiviral gene delivery of a dominant negative ERK5 or dominant negative MAP kinase kinase 5 reduced the number of neurons generated from rat cortical progenitor cells in culture, whereas constitutive activation of ERK5 increased the production of neurons. Furthermore, when cortical progenitor cells were treated with ciliary neurotrophic factor, which induces precocious glial differentiation, ERK5 activation still promoted neuronal fate while suppressing glial differentiation. Our data also indicate that ERK5 does not directly regulate proliferation or apoptosis of cultured cortical progenitors. We conclude that ERK5 is necessary and sufficient to stimulate the generation of neurons from cortical progenitors. These results suggest a previously uncharacterized function for ERK5 signaling during brain development and raise the interesting possibility that extrinsic factors may instruct cortical progenitors to become neurons by activating the ERK5 pathway.

Animals↗

PubMed2006

[Effect of kaempferol on the pharmacokinetics of nifedipine in rats].

OBJECTIVE: To investigate the effect of kaempferol on the pharmacokinetics of nifedipine (NFP) in rats. METHODS: Twenty male SD rats, weighing 220-260 g, were distributed randomly into 4 groups. The animals were fasted, but allowed free access to water for 12 h before the administration of drugs. NFP dissolved in corn oil was administered via gastric intubation to the rats in control group at a dose of 10 mg/kg. Kaempferol was administered orally to the other three groups with dose of 5, 10, 15 mg/kg, respectively, followed by oral administration of NFP 10 mg/kg. Blood samples were collected through tail vein in heparinized plastic microcentrifuge tubes before and after drug administration. The plasma concentration of NFP was monitored with reversed phase high-performance liquid chromatography (RP-HPLC). Nimodipine was used as the internal standard. Statistical data evaluation was performed with Student's t-test and one-way analysis of variances. RESULTS: The maximal plasma concentration (C(max)) of the three treated groups were 0.51, 0.70 and 0.81 microg/ml, respectively. The area under the concentration-time curve (AUC(0-8)) were 1.81, 2.83 and 3.63 microg/(h.ml(-1)), respectively. The C(max), AUC(0-8) and the mean retention time (MRT(0-8)) of NFP were significantly increased by simultaneous oral treatment with kaempferol (P<0.01). On the other hand, there were no significant differences in the mean peak value time in plasma (T(max)) and the elimination half-life (t1/2(ke)) between the control and the treated groups. CONCLUSION: The concomitant oral use of kaempferol with NFP may influence the pharmacokinetic parameters of NFP in rats, which suggests that kaempferol might reduce the first-pass metabolism of NFP.

Animals↗

PubMed2006

[Effectiveness and safety of recombinant human interleukin-11 in the treatment of chemotherapy-induced thrombocytopenia].

OBJECTIVE: To investigate the effectiveness and safety of domestically produced recombinant human interleukin 11 (rhIL-11) for the treatment of chemotherapy- induced thrombocytopenia. METHODS: A total of 32 solid cancer patients who developed chemotherapy-induced thrombocytopenia ( _70 x 10(9)/L) after the first cycle of chemotherapy was studied by self-cross control. The patients were given subcutaneous injection of rhIL-11 (25 microg x kg(-1) x d(-1)) for 7 to 14 consecutive days or until platelet count > or = 100 x 10(9)/L during the second cycle of chemotherapy using the identical regimen as in the first cycle. RESULTS: The mean platelet count of the patients after rhIL-11 treatment was higher at different time points during the second cycle of chemotherapy than that during the first cycle of chemotherapy with the mean platelet count of (110.2 +/- 53.5) x 10(9)/L in the first cycle of chemotherapy versus (55.6 +/- 46.8) x 10(9)/L in the second cycle of chemotherapy (P < 0. 01). Patients with platelet count < or = 50 x 10(9)/L was 4/32 (12.5%) in the first cycle of chemotherapy and 12/32 (37.5%) in the second cycle of chemotherapy (P < 0.01). The time recovery to the normal platelet count was 2 - 18 days (median 5 days) in the first cycle of chemotherapy versus 5 - 27 days (median 12 days) in the second cycle of chemotherapy (P < 0.01). The case/frequency of the platelet transfusion was 2/2 in the first cycle of chemotherapy, while it was 7/9 in the second cycle of chemotherapy (P < 0.01). The major adverse reactions relative to rhIL-11 treatment were fatigue, myalgia/arthralgia, ache, headache, palpitation, edema and fever, most of which could be relieved automatically without any specific treament. However, some 3 grade side effects such as fatigue, myalgia/arthralgia and headache needed proper medication. CONCLUSION: rhIL-11 is safe and effective for chemotherapy-induced thrombocytopenia with mild and manageable side effects.

Adult↗

PubMed2005

Tyrosine phosphorylation of K(ir)3.1 in spinal cord is induced by acute inflammation, chronic neuropathic pain, and behavioral stress.

Tyrosine phosphorylation is an important means of regulating ion channel function. Our previous gene expression studies using the Xenopus laevis oocyte system suggested that tyrosine phosphorylation of G-protein-gated inwardly rectifying potassium channels (K(ir)3 or GIRK) suppressed basal channel conductance and accelerated channel deactivation. To assess whether similar mechanisms regulate K(ir)3 function in mammalian cells, we developed and characterized a phosphoselective antibody recognizing K(ir)3.1 phosphorylated at tyrosine 12 in the N-terminal domain and then probed for evidence of K(ir)3.1 phosphorylation in cultured mammalian cells and spinal cord. The antibody was found to discriminate between the phospho-Tyr(12) of K(ir)3.1 and the native state in transfected cell lines and in primary cultures of mouse atria. Following either mouse hindpaw formalin injection or sciatic nerve ligation, pY12-K(ir)3.1 immunoreactivity was enhanced unilaterally in the superficial layers of the spinal cord dorsal horn, regions previously described as expressing K(ir)3.1 channels. Mice lacking K 3.1 following targeted gene disruption did not show specific pY12-K(ir)3.1 immunoreactivity after sciatic nerve ligation. Further, mice exposed to repeatedly forced swim stress showed bilateral enhancement in pY12-K(ir)3.1 in the dorsal horn. This study provides evidence that K(ir)3 tyrosine phosphorylation occurred during acute and chronic inflammatory pain and under behavioral stress. The reduction in K(ir)3 channel activity is predicted to enhance neuronal excitability under physiologically relevant conditions and may mediate a component of the adaptive physiological response.

Animals↗

PubMed2005

Both the phosphoinositide and receptor binding activities of Dab1 are required for Reelin-stimulated Dab1 tyrosine phosphorylation.

Reelin-stimulated tyrosine phosphorylation of the Dab1 adaptor protein is required during brain development for Reelin-dependent neuron positioning in the cerebral cortex and various other laminated regions. Dab1 contains an amino-terminal PTB/PI domain through which it can bind to Reelin receptors and membrane phosphoinositides. The relative contributions of these binding activities were unknown. Here, we identify a mutation in the PTB domain of Dab1 that inhibits membrane localization without inhibiting receptor binding. In neurons, this mutation reduces both basal and Reelin-stimulated Dab1 tyrosine phosphorylation. In contrast, a mutation that inhibits receptor binding reduces Reelin-stimulated but not basal tyrosine phosphorylation. These results support a model in which phospholipids recruit Dab1 to membranes but do not play a direct role in relaying the Reelin signal, while direct Dab1-receptor interaction is responsible for relaying the Reelin signal but not for membrane recruitment.

Animals↗

PubMed2005

Role for medullary pain facilitating neurons in secondary thermal hyperalgesia.

The rostral ventromedial medulla (RVM) has recently received considerable attention in efforts to understand mechanisms of hyperalgesia and persistent pain states. Three classes of neurons can be identified in the RVM based on responses associated with nocifensive reflexes: on cells, off cells, and neutral cells. There is now direct evidence that on cells exert a net facilitating effect on spinal nociception and that off cells depress nociception. These experiments tested whether the secondary hyperalgesia produced by topical application of mustard oil involves an activation of on cells in RVM. Firing of a characterized RVM neuron and the latencies of withdrawal reflexes evoked by noxious heat were recorded in lightly anesthetized rats before and after application of mustard oil to the shaved skin of the leg above the knee. Mineral oil was applied as a control. Mustard oil produced a significant increase in ongoing and reflex-related discharge of on cells, as well as a decrease in the activity of off cells. neutral cell firing was uniformly unchanged after application of mustard oil. The alterations in on and off cell firing were associated with a significant decrease in the latency to withdraw the paw of the treated limb from the heat stimulus, and this hyperalgesia was blocked by microinjection of lidocaine within the RVM. Withdrawals evoked by heating the contralateral hindpaw, forepaw, and tail were unchanged after mustard oil application. These experiments support a pronociceptive role for on cells and suggest that these neurons contribute to secondary hyperalgesia in inflammation.

Action Potentials↗

PubMed2005

A digital atlas to characterize the mouse brain transcriptome.

Massive amounts of data are being generated in an effort to represent for the brain the expression of all genes at cellular resolution. Critical to exploiting this effort is the ability to place these data into a common frame of reference. Here we have developed a computational method for annotating gene expression patterns in the context of a digital atlas to facilitate custom user queries and comparisons of this type of data. This procedure has been applied to 200 genes in the postnatal mouse brain. As an illustration of utility, we identify candidate genes that may be related to Parkinson disease by using the expression of a dopamine transporter in the substantia nigra as a search query pattern. In addition, we discover that transcription factor Rorb is down-regulated in the barrelless mutant relative to control mice by quantitative comparison of expression patterns in layer IV somatosensory cortex. The semi-automated annotation method developed here is applicable to a broad spectrum of complex tissues and data modalities.

Anatomy, Artistic↗

PubMed2005

Distinct roles of oxidative stress and antioxidants in the nucleus dorsalis and red nucleus following spinal cord hemisection.

Oxidative stress plays an important role in the pathogenesis of neurodegeneration after the acute central nervous system injury. We reported previously that increased nitric oxide (NO) production following spinal cord hemisection tends to lead to neurodegeneration in neurons of the nucleus dorsalis (ND) that normally lacks expression of neuronal NO synthase (nNOS) in opposition to those in the red nucleus (RN) that constitutively expresses nNOS. We wondered whether oxidative stress could be a mechanism underlying this NO involved neurodegeneration. In the present study, we examined oxidative damage evaluated by the presence of 4-hydroxynonenal (HNE) and iron accumulation and expression of putative antioxidant enzymes heme oxygenase-1 (HO-1) and superoxide dismutase (SOD) in neurons of the ND and RN after spinal cord hemisection. We found that HNE expression was induced in neurons of the ipsilateral ND from 1 to 14 days following spinal cord hemisection. Concomitantly, iron staining was seen from 7 to 14 days after lesion. HO-1, however, was only transiently induced in ipsilateral ND neurons between 3 and 7 days after lesion. In contrast to the ND neurons, HNE was undetectable and iron level was unaltered in the RN neurons after spinal cord hemisection. HO-1, SOD-Cu/Zn and SOD-Mn were constitutively expressed in RN neurons, and lesion to the spinal cord did not change their expression. These results suggest that oxidative stress is involved in the degeneration of the lesioned ND neurons; whereas constitutive antioxidant enzymes may protect the RN neurons from oxidative damage.

Aldehydes↗

PubMed2005

Theoretically modeling microarray with the chemical equilibrium and thermodynamics.

To date, the idea that microarray may shed the light on cellular processes by identifying groups of genes that appear to be co-expressed seems to remain a dream. This is partly because that there are some blank (meaning the knowledge is unavailable) or even erroneous areas in the fundamental theory in this field. This paper attempts to present the digest of microarray hybridization system with chemical thermodynamics, theoretically clarifying some misunderstandings and looking for answers to some critical questions around this technology, such as the mechanisms and conditions of quantitative measuring by hybridization reaction, the reasons of inconsistency of the data and the analysis results and the solutions, how to analyze the data, etc. A theoretical model for the next generation of microarray is proposed. We believe that this model is universal, laying the foundation for microarray technology from array design through the data analysis.

Computer Simulation↗

PubMed2005

[Determination of amino acids in fu fang banlangen granulae by a pre-column derivatization RP-HPLC method].

OBJECTIVE: To establish a pre-column derivatization reversed-phase high-performance liquid chromatographic method for the determination of amino acids, which was known as the characteristic constituents of Fu Fang Banlangen Granulae. METHODS: We determined the amino acids in alkalescence by a pre-column derivatization of DNFB. NaAc buffer (pH 6.4)-Acetonitrile (850:150) was used as the mobile phase on a SinoChrom ODS-BP column. The detector was operated at 360 nm. RESULTS: The method was carried out over the range of 0.627 - 5. 016 microg for Arg and 0.874 - 7.000 microg for Pro. The recoveries were 97.7% with the RSD = 2.0% for Arg and 97.7% with the RSD = 1.5% for Pro. CONCLUSIONS: The method has good accuracy and repeatability and it can be used for the quality control of Fu Fang Banlangen Granulae.

Amino Acids↗

PubMed2004

Neuropathic pain activates the endogenous kappa opioid system in mouse spinal cord and induces opioid receptor tolerance.

Release of endogenous dynorphin opioids within the spinal cord after partial sciatic nerve ligation (pSNL) is known to contribute to the neuropathic pain processes. Using a phosphoselective antibody [kappa opioid receptor (KOR-P)] able to detect the serine 369 phosphorylated form of the KOR, we determined possible sites of dynorphin action within the spinal cord after pSNL. KOR-P immunoreactivity (IR) was markedly increased in the L4-L5 spinal dorsal horn of wild-type C57BL/6 mice (7-21 d) after lesion, but not in mice pretreated with the KOR antagonist nor-binaltorphimine (norBNI). In addition, knock-out mice lacking prodynorphin, KOR, or G-protein receptor kinase 3 (GRK3) did not show significant increases in KOR-P IR after pSNL. KOR-P IR was colocalized in both GABAergic neurons and GFAP-positive astrocytes in both ipsilateral and contralateral spinal dorsal horn. Consistent with sustained opioid release, KOR knock-out mice developed significantly increased tactile allodynia and thermal hyperalgesia in both the early (first week) and late (third week) interval after lesion. Similarly, mice pretreated with norBNI showed enhanced hyperalgesia and allodynia during the 3 weeks after pSNL. Because sustained activation of opioid receptors might induce tolerance, we measured the antinociceptive effect of the kappa agonist U50,488 using radiant heat applied to the ipsilateral hindpaw, and we found that agonist potency was significantly decreased 7 d after pSNL. In contrast, neither prodynorphin nor GRK3 knock-out mice showed U50,488 tolerance after pSNL. These findings suggest that pSNL induced a sustained release of endogenous prodynorphin-derived opioid peptides that activated an anti-nociceptive KOR system in mouse spinal cord. Thus, endogenous dynorphin had both pronociceptive and antinociceptive actions after nerve injury and induced GRK3-mediated opioid tolerance.

Animals↗

PubMed2004

Prolactin-releasing peptide affects pain, allodynia and autonomic reflexes through medullary mechanisms.

Prolactin-releasing peptide (PrRP) and neuropeptide FF (NPFF) are RF-amide peptides expressed in brain areas involved in pain modulation. NPFF displays multiple effects on acute, inflammatory and neuropathic pain. The potential role of PrRP in pain was addressed by intrathecal and intracerebral injections of PrRP on pain-related responses in both neuropathic and normal rats. Particularly in the dorsal medulla, PrRP produced significant antinociception in normal rats and an antiallodynic effect in neuropathic rats. To understand the basis of PrRP-induced pain modulation, distributions of PrRP, PrRP receptor, and NPFF were compared in the rat central nervous system. PrRP and NPFF mRNA were expressed in different parts of the nucleus of the solitary tract. In the medulla, PrRP receptor mRNA expression was abundant only in area postrema. Of the peptides studied, only NPFF mRNA was found in the dorsal horn of the spinal cord and spinal nucleus of the trigeminal nerve. PrRP-immunoreactivity corresponded to the mRNA distribution. Even if the neuronal groups producing NPFF and PrRP were distinct, the fiber networks immunoreactive for PrRP and NPFF overlapped. The results show that PrRP modulates nociception due to supraspinal rather than spinal action, and that its antinociceptive mechanism differs from that previously characterized for NPFF.

Animals↗

PubMed2004

Molecular mechanisms of gonadotropin-releasing hormone neuronal migration.

Gonadotropin-releasing hormone (GnRH) neurons originate in the nasal compartment, migrate along olfactory nerves to the cribriform plate and then diverge caudally to the forebrain to reach their final destination in the hypothalamus. Here, GnRH neurons are dispersed in a network that synchronously releases GnRH in a pulsatile manner to activate pituitary gonadotropin production. Gonadotropins in turn promote gametogenesis and steroidogenesis from the gonad, ensuring reproductive competence. Failure of GnRH neurons to migrate normally results in deficient activation of the reproductive axis and delayed or absent pubertal maturation. The exact mechanisms that direct GnRH neuronal migration are under active investigation. This article will review new information concerning factors regulating GnRH neuronal migration and the intracellular signaling pathways involved in this process.

Animals↗

PubMed2004

An improved, inexpensive procedure for the large-scale purification of recombinant human erythropoietin.

A rapid and simple chromatographic procedure has been developed for the large-scale purification of therapeutic-grade rHuEPO (recombinant human erythropoietin) from medium-conditioned cell cultures, which includes ion-exchange, hydrophobic-interaction and gel-filtration chromatography. A combination of these well-connected steps results in highly purified rHuEPO (> 99%), as revealed by SDS/PAGE and HPLC analyses, with a total yield of 38%. The specific activity of purified rHuEPO was 160,104 i.u./mg. Immunoblotting studies revealed that the protein possesses native EPO immunity. N-terminal sequencing of rHuEPO shows that the first 15 amino acids coincide with those of native EPO reported previously.

Animals↗