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Yi Zhu

Publications and source records attributed to Yi Zhu.

At least 19 recordsLinked to original sources
PubMed2026

High-frequency contralesional dorsal premotor cortex and low-frequency contralesional primary motor cortex rTMS in subacute stroke with severe upper limb impairment: comparable motor outcomes and differential regional degree centrality changes.

BACKGROUND: The contralesional dorsal premotor cortex has been proposed as a potential neuromodulatory target for patients with severe upper limb impairment due to subacute ischemic stroke. This proof-of-concept study aimed to compare behavioral outcomes and resting-state neuroimaging findings between high-frequency repetitive transcranial magnetic stimulation (rTMS) over the contralesional dorsal premotor cortex and guideline-supported low-frequency stimulation over the contralesional primary motor cortex. METHODS: In this randomized trial, 46 patients with severe upper limb impairment in the subacute stage after ischemic stroke were randomly assigned to receive either high-frequency rTMS over the contralesional dorsal premotor cortex or low-frequency rTMS over the contralesional primary motor cortex. Low-frequency stimulation over the contralesional primary motor cortex served as an evidence-supported active comparator for poststroke upper limb motor recovery. Stimulation was administered five times per week for two weeks using magnetic resonance imaging-guided neuronavigation. All participants received concurrent standard rehabilitation therapy. The primary outcome was the Fugl-Meyer Assessment for Upper Extremity. Secondary outcomes included the Arm Subscore of the Motricity Index, the Hong Kong version of the Functional Test for the Hemiplegic Upper Extremity, the Modified Barthel Index, and resting-state functional magnetic resonance imaging-derived degree centrality. RESULTS: Both groups showed significant improvements in the primary and secondary behavioral measures (p&#x202f;<&#x202f;0.01), with no significant between-group differences in the magnitude of change (p&#x202f;>&#x202f;0.05). In neuroimaging analyses, patients receiving high-frequency rTMS over the contralesional dorsal premotor cortex showed significantly greater degree centrality changes in the ipsilesional middle occipital gyrus, contralesional medial superior frontal gyrus, and contralesional middle frontal gyrus than those receiving low-frequency rTMS over the contralesional primary motor cortex (p&#x202f;<&#x202f;0.05). Within the high-frequency stimulation group, degree centrality changes in the ipsilesional middle occipital gyrus were positively correlated with improvements in the Fugl-Meyer Assessment for Upper Extremity (r&#x202f;=&#x202f;0.619, false discovery rate-corrected p&#x202f;=&#x202f;0.018). CONCLUSIONS: High-frequency rTMS over the contralesional dorsal premotor cortex produced behavioral improvements comparable to guideline-supported low-frequency rTMS over the contralesional primary motor cortex, without establishing superiority or formal non-inferiority. Exploratory neuroimaging analyses showed greater degree centrality changes in the ipsilesional middle occipital gyrus after high-frequency premotor stimulation, and these changes correlated with upper-limb motor improvement. These findings support further investigation of contralesional dorsal premotor cortex-targeted high-frequency rTMS for severe subacute post-stroke upper limb impairment. REGISTRATION: URL: http://www.chictr.org.cn; Unique identifier: ChiCTR2000038049.

Humans↗
PubMed2026

Allelic variation in UVR8 modulates thermotolerance-yield tradeoffs in plants.

Industrial activities have driven stratospheric ozone depletion, increasing surface UV-B radiation while exacerbating global warming. These changes limit crop productivity, alter species distributions, and disrupt plant metabolic processes, but the mechanisms linking energy signaling to heat-stress responses remain unclear. Here, we identify the photoreceptor UV RESISTANCE LOCUS 8b (OsUVR8b) as a substrate of SNF1-related protein kinase 1&#xa0;(SnRK1) in rice and reveal a natural variation at its SnRK1-mediated phosphorylation site (Ser177) that is correlated with adaptation to tropical climates. The thermotolerant OsUVR8bAla177 accessions show geographic enrichment in low-latitude regions with elevated temperatures. Functional validation through prime editing demonstrated that a Ser177-to-Ala177 substitution enhances heat tolerance, whereas the reverse edit compromises it. Mechanistically, OsUVR8bSer177 exhibits reduced stability and an impaired capacity for scavenging reactive oxygen species under heat stress. The regulatory function of the OsUVR8b Ser177 phosphorylation site, a molecular switch that governs UVR8 stability and thermotolerance, can be functionally re-established across rice, Arabidopsis, tobacco, and soybean, indicating its preservation during domestication. Notably, OsUVR8bSer177 maintains higher fertility and yield under non-stress conditions, indicating a tradeoff between heat adaptation and productivity. Our findings thus establish this switch as a key regulator of the yield-resilience balance and a promising target for breeding of climate-resilient crops.

Thermotolerance↗
PubMed2025

Efficacy of esketamine in reducing nausea and vomiting after anesthesia: a systematic review and meta-analysis of randomized controlled trials.

BACKGROUND: Postoperative nausea and vomiting (PONV) are significant perioperative challenges. This study evaluated the efficacy of perioperative esketamine in preventing PONV. MATERIALS AND METHODS: We systematically searched Embase, PubMed, Web of Science, and the Cochrane Library from inception to August 2025 for randomized controlled trials investigating the effect of perioperative esketamine on PONV. The primary outcome was PONV incidence. Secondary outcomes included time to first flatus, postoperative pain degree, anxiety scores, agitation, anesthesia recovery time, and post-anesthesia care unit (PACU) stay duration. Data were analyzed using RevMan 5.4 and STATA 15.0 software. Sensitivity and subgroup analyses were performed to assess result stability and explore potential sources of heterogeneity. RESULTS: Thirty-eight randomized trials (3,425 patients) were included. Esketamine reduced the risk of nausea (RR=0.69, 95% CI: 0.53-0.90) and vomiting (RR=0.75, 95% CI: 0.57-0.98), shortened time to first flatus (SMD=-0.81, 95% CI: -1.48 to -0.15), and decreased rescue analgesic needs within 2 days (SMD=0.32, 95% CI: 0.2-0.5). However, it prolonged anesthesia recovery time (SMD=0.97, 95% CI: 0.28-1.67) and PACU stay (SMD=0.76, 95% CI: 0.27-1.26). CONCLUSIONS: Perioperative esketamine may reduce PONV and aid gastrointestinal recovery, but its potential to delay anesthesia recovery and PACU discharge requires consideration. Further studies are needed to clarify its risk-benefit profile. DATE OF FIRST SUBMISSION TO PROSPERO: 10 March 2024. DATE OF THE START OF STUDY SCREENING AGAINST ELIGIBILITY CRITERIA: 21 March 2024.

Humans↗
PubMed2006

Characterization of ResDE-dependent fnr transcription in Bacillus subtilis.

The ResD-ResE signal transduction system is required for transcription of genes involved in aerobic and anaerobic respiration in Bacillus subtilis. Phosphorylated ResD (ResD approximately P) interacts with target DNA to activate transcription. A strong sequence similarity was detected in promoter regions of some ResD-controlled genes including fnr and resA. Single-base substitutions in the fnr and resA promoters were performed to determine a ResD-binding sequence. DNase I footprinting analysis indicated that ResD approximately P itself does not bind to fnr, but interaction of ResD approximately P with the C-terminal domain of the alpha subunit (alphaCTD) of RNA polymerase (RNAP) facilitates cooperative binding of ResD approximately P and RNAP, thereby increasing fnr transcription initiation. Consistent with this result, amino acid substitutions in alphaCTD, such as Y263A, K267A, A269I, or N290A, sharply reduced fnr transcription in vivo, and the K267A alphaCTD protein, unlike the wild-type protein, did not increase ResD approximately P binding to the fnr promoter. Amino acid residues of alphaCTD required for ResD-dependent fnr transcription, with the exception of N290, which may interact with DNA, constitute a distinct surface, suggesting that these residues likely interact with ResD approximately P.

Amino Acid Substitution↗
PubMed2006

Arsenic trioxide, a potent inhibitor of NF-kappaB, abrogates allergen-induced airway hyperresponsiveness and inflammation.

BACKGROUND: Overactivation of nuclear factor kappaB (NF-kappaB) orchestrates airway eosinophilia, but does not dampen airway hyperresponsiveness in asthma. NF-kappaB repression by arsenic trioxide (As2O3) contributes to apoptosis of eosinophils (EOS) in airways. Here we provide evidence that As2O3 abrogates allergen (OVA)-induced airway eosinophilia by modulating the expression of IkappaBalpha, an NF-kappaB inhibitory protein, and decreases the airway hyperresponsiveness. METHODS: Using a murine model of asthma, the airway hyperresponsiveness was conducted by barometric whole-body plethysmography. Airway eosinophilia, OVA-specific IgE in serum, and chemokine eotaxin and RANTES (regulated upon activation, normal T cell expressed and secreted) in bronchoalveolar lavage fluid were measured by lung histology, Diff-Quick staining, and ELISA. Chemokine-induced EOS chemotactic activity was evaluated using EOS chemotaxis assay. Electrophoretic mobility shift assay and Western blot analysis were performed to assess pulmonary NF-kappaB activation and IkappaBalpha expression, respectively. RESULTS: As2O3 attenuated the allergen-induced serum IgE, chemokine expression of eotaxin and RANTES, and the EOS recruitment in bronchoalveolar lavage fluid, which is associated with an increased IkappaBalpha expression as well as a decreased NF-kappaB activation. Also, As2O3 suppressed the chemotaxis of EOS dose-dependently in vitro. Additionally, As2O3 significantly ameliorated the allergen-driven airway hyperresponsiveness, the cardinal feature underlying asthma. CONCLUSION: These findings demonstrate an essential role of NF-kappaB in airway eosinophilia, and illustrate a potential dissociation between airway inflammation and hyperresponsiveness. As2O3 likely exerts its broad anti-inflammatory effects by suppression of NF-kappaB activation through augmentation of IkappaBalpha expression in asthma.

Allergens↗
PubMed2006

ROS and NF-kappaB but not LXR mediate IL-1beta signaling for the downregulation of ATP-binding cassette transporter A1.

ATP-binding cassette transporter A1 (ABCA1), a pivotal regulator of cholesterol efflux from cells to apolipoproteins, plays an important role in cholesterol homeostasis. As an inflammatory factor, IL-1beta has been shown to downregulate ABCA1 in macrophages and facilitates foam cell formation. However, the molecular mechanism underlining the downregulated ABCA1 by IL-1beta is still elusive. In the present study, we demonstrated that IL-1beta downregulated ABCA1 but not ABCG1 at mRNA and protein levels in a time- and dose-dependent manner in THP-1 and A549 cells. IL-1beta attenuated ABCA1 promoter activity through an LXR (liver X receptor)-independent pathway, since IL-1beta did not alter the expression and activities of LXRalpha/beta, and deletion of the LXR responsive element from the ABCA1 promoter failed to reverse the IL-1beta effect. In contrast, NF-kappaB inhibition by pyrrolidine dithiocarbamate and MG132 prevented the suppression of ABCA1 by IL-1beta. Cotransfection with ABCA1 luciferase reporter and the expression plasmids of Rel A decreased ABCA1 promoter activities. An adenovirus expressing NF-kappaB inhibitor subunit-alpha inhibited NF-kappaB activities and also reversed the IL-1beta effect at the promoter activity and protein levels of ABCA1. In addition, IL-1beta could induce the production of reactive oxygen species (ROS), and N-acetyl-L-cysteine, a scavenger of ROS, reversed the decreased level of ABCA1 induced by IL-1beta. H(2)O(2) decreased ABCA1 at the mRNA and protein levels and the promoter activity. Thus our data provide strong evidence that ROS and NF-kappaB, but not LXR, mediate the IL-1beta-induced downregulation of ABCA1 via a novel transcriptional mechanism, which might play an important role of proinflammation in the alteration of lipid metabolism.

ATP Binding Cassette Transporter 1↗
PubMed2006

Statins activate AMP-activated protein kinase in vitro and in vivo.

BACKGROUND: Statins exert pleiotropic effects on the cardiovascular system, in part through an increase in nitric oxide (NO) bioavailability. AMP-activated protein kinase (AMPK) plays a central role in controlling energy and metabolism homeostasis in various organs. We therefore studied whether statins can activate AMPK, and if so, whether the activated AMPK regulates nitric oxide (NO) production and angiogenesis mediated by endothelial NO synthase, a substrate of AMPK in vascular endothelial cells. METHODS AND RESULTS: Western blotting of protein extracts from human umbilical vein endothelial cells treated with atorvastatin revealed increased phosphorylation of AMPK at Thr-172 in a time- and dose-dependent manner. The AMPK activity, assessed by SAMS assay, was also increased accordingly. The phosphorylation of acetyl-CoA carboxylase at Ser-79 and of endothelial NO synthase at Ser-1177, 2 putative downstream targets of AMPK, was inhibited by an adenovirus that expressed a dominant-negative mutant of AMPK (Ad-AMPK-DN) and compound C, an AMPK antagonist. The positive effects of atorvastatin, including NO production, cGMP accumulation, and in vitro angiogenesis in Matrigel, were all blocked by Ad-AMPK-DN. Mice given atorvastatin through gastric gavage showed increased AMPK, acetyl-CoA carboxylase, and endothelial NO synthase phosphorylation in mouse aorta and myocardium. CONCLUSIONS: Statins can rapidly activate AMPK via increased Thr-172 phosphorylation in vitro and in vivo. Such phosphorylation results in endothelial NO synthase activation, which provides a novel explanation for the pleiotropic effects of statins that benefit the cardiovascular system.

AMP-Activated Protein Kinases↗
PubMed2006

[Forensic identification of floating shoulder injury].

OBJECTIVE: To discuss forensic identification of floating shoulder injury (FSI). METHODS: To analyze fifteen cases of FSI which were accepted from Jan. 1993 to Jan. 2006, including 15 shoulder neck fracture, 13 clavide stem fracture and 2 distal end clavide fracture, the function of shoulder joint was evaluated six months after injure considering the following three aspects: result of forensic examination such as X-ray photograph, CT and MRI, the injurers' symptom, objective sign and joint function, shoulder joint territory, degree of pain and local muscle power. RESULTS: Basing on the curative effect standard of Herscovic, all cases were divided into good. Modest, worst, which included 2, 4, 9 cases respectively; referring the standard of GA35-92, GB18667-2002, all cases were divided into six, seven, eight, nine and ten degree, which included 2,9,2,1,1 cases respectively. CONCLUSION: As a special powerful injure, FSI always companied with concurrent and multiple injure, and characterized by missed, incorrect and delayed diagnosis and infelicitous treatment, which lead to the high frequency and degree of injure. To prevent missed and incorrect forensic identification, we should have a full realization of the particularity of FSI, and evaluate the function of shoulder all-sidely, objectively and synseticaly.

Accidents, Traffic↗
PubMed2006

Expression of LPL in endothelial-intact artery results in lipid deposition and vascular cell adhesion molecule-1 upregulation in both LPL and ApoE-deficient mice.

OBJECTIVE: Overexpression of lipoprotein lipase (LPL) in deendothelialized artery led to profound localized lipid deposition. In this study the role of LPL in atherogenesis in endothelial-intact carotid arteries was assessed in genetically hyperlipidemic LPL- and ApoE-deficient mice. METHODS AND RESULTS: Human wild-type LPL (hLPLwt), catalytically inactive LPL (hLPL194), or control alkaline phosphatase (hAP) were expressed in endothelial-intact carotid arteries via adenoviral vectors. Compared with Ad-hAP, lipid deposition in the arterial wall increased 10.0- and 5.1-fold for Ad-hLPLwt and Ad-hLPL194 in LPL-deficient mice, and 10.6- and 6.2-fold in ApoE-deficient mice, respectively. Vascular cell adhesion molecule-1 (VCAM-1) was upregulated in Ad-hLPLwt and Ad-hLPL194 transferred arteries. CONCLUSIONS: Endothelial cell associated LPL, either active or inactive, in the arterial wall is a strong proatherosclerotic factor in both LPL- and ApoE-deficient mice.

Animals↗
PubMed2006

Role of redox factor-1 in hyperhomocysteinemia-accelerated atherosclerosis.

Hyperhomocysteinemia (HHcy) is an independent risk factor for atherosclerosis. We have previously shown that homocysteine can induce monocyte chemoattractant protein-1 (MCP-1) secretion via reactive oxygen species (ROS) in human monocytes in vitro. In the present study, we investigated whether redox factor-1 (Ref-1) is involved in HHcy-accelerated atherosclerosis. We used a mild HHcy animal model, aortic roots and peritoneal macrophages were isolated for immunohistochemistry and Western blotting, from apoE-/- and C57BL/6J mice fed a high Hcy diet (1.8 g/L) for 4 or 12 weeks. Four-week HHcy apoE-/- mice showed more plaques and significantly increased immunostaining of Ref-1 and MCP-1 in foam cells, and HHcy mice showed enhanced Ref-1 expression in peritoneal macrophages. To explore the mediating mechanism, incubation with Hcy (100 microM) increased Ref-1 protein level and translocation in human monocytes in vitro. In addition, Hcy-induced NADPH oxidase activity mediated the upregulation of Ref-1. Furthermore, overexpressed Ref-1 upregulated NF-kappaB and MCP-1 promoter activity, and antisense Ref-1 reduced Hcy-induced NF-kappaB DNA-binding activity and MCP-1 secretion. These data indicate that Hcy-induced ROS upregulate the expression and translocation of Ref-1 via NADPH oxidase, and then Ref-1 increases NF-kappaB activity and MCP-1 secretion in human monocytes/macrophages, which may accelerate the development of atherosclerosis.

Animals↗
PubMed2006

Cholesterol loading increases the translocation of ATP synthase beta chain into membrane caveolae in vascular endothelial cells.

Caveolae and its structural protein caveolin-1 (Cav-1) are abundant in vascular endothelial cells (ECs) and have been suggested to contribute to cell signaling and cholesterol trafficking. This study investigated the effect of cholesterol on the movement of caveolae-related proteins in human umbilical vein ECs with use of caveolae functional proteomics. After cholesterol exposure to ECs for 2 to 4 h, caveolae were isolated and separated on 2-D protein gels. Among 40 protein spots revealed in caveolae fractions, the ATP synthase beta subunit (ATPS-beta), one of the 3 proteins enriched by cholesterol in caveolae, was confirmed by western blotting and confocal microscopy. Further, cholesterol exposure increased the level of ATPS-beta, along with Cav-1 and cholesterol in caveolae. These effects could be blocked by cytochalasin B, an actin cytoskeleton disruptor. ATPS-beta was physically associated with Cav-1, as demonstrated by co-immunoprecipitation and GST-Cav-1 fusion protein pull-down assay. Cholesterol increased the extracellular ATP release mediated by ATPS-beta, since this action could be blocked by piceatannol or oligomycin, ATPS inhibitors. Thus, the ectopic localization of ATPS-beta may participate in the energy balance of cells in response to the change in intracellular cholesterol levels.

Caveolae↗
PubMed2006

Maternally transmitted diabetes mellitus associated with the mitochondrial tRNA(Leu(UUR)) A3243G mutation in a four-generation Han Chinese family.

We report here the characterization of a four-generation Han Chinese family with maternally transmitted diabetes mellitus. Six (two males/four females) of eight matrilineal relatives in this family exhibited diabetes. The age of onset in diabetes varies from 15 years to 33 years, with an average of 26 years. Two of affected matrilineal relatives also exhibited hearing impairment. Molecular analysis of mitochondrial DNA (mtDNA) showed the presence of heteroplasmic tRNA(Lue(UUR)) A3243G mutation, ranging from 35% to 58% of mutations in blood cells of matrilineal relatives. The levels of heteroplasmic A3243G mutation seem to be correlated with the severity and age-at-onset of diabetes in this family. Sequence analysis of the complete mitochondrial genome in this pedigree revealed the presence of the A3243G mutation and 38 other variants belonging to the Eastern Asian haplogroup M7C. However, none of other mtDNA variants are evolutionarily conserved and implicated to have significantly functional consequence. Thus, the A3243G mutation is the sole pathogenic mtDNA mutation associated with diabetes in this Chinese family.

Adolescent↗
PubMed2006

Design and synthesis of butynyloxyphenyl beta-sulfone piperidine hydroxamates as TACE inhibitors.

A series of butynyloxyphenyl beta-sulfone piperidine hydroxamate TACE inhibitors was designed and synthesized. The resulting structure-activity relationship and MMP selectivity of the series were examined. Of the compounds investigated, 17s has excellent in vitro potency against isolated TACE enzyme, shows good selectivity over MMP-1, -2, -7, -8, -9, -13, and -14, and oral activity in an in vivo mouse model of TNF-alpha production.

ADAM Proteins↗
PubMed2006

Calcitonin gene-related peptide inhibits interleukin-1beta-induced endogenous monocyte chemoattractant protein-1 secretion in type II alveolar epithelial cells.

As important multifunctional cells in the lung, alveolar epithelial type II (AEII) cells secrete numerous chemokines on various stimuli. Our previous data showed that AEII cells also express the neuropeptide calcitonin gene-related peptide (CGRP) and the proinflammatory factor interleukin (IL)-1beta induces CGRP secretion in the A549 human AEII cell line. In the present study, the CGRP-1 receptor antagonist human (h)CGRP(8-37) (0.1-1 nM) greatly amplified the production of IL-1beta-induced monocyte chemoattractant protein (MCP)-1. The inhibition of CGRP expression by small interfering RNA significantly increased MCP-1 secretion on IL-1beta stimulation. However, exogenous hCGRP (10-100 nM) suppressed IL-1beta-evoked MCP-1 secretion in MCP-1 promoter activity, and CGRP gene stably transfected cell clones significantly inhibited both the mRNA and protein levels of MCP-1 induced by IL-1beta. These data imply that AEII-derived CGRP suppressed IL-1beta-induced MCP-1 secretion in an autocrine/paracrine mode. Subsequent investigation revealed that CGRP inhibited IL-1beta-evoked NF-kappaB activity by suppressing IkappaBalpha phosphorylation and degradation. Moreover, CGRP attenuated IL-1beta-induced reactive oxygen species (ROS) formation, the early event in proinflammatory factor signaling. We previously showed that the CGRP inhibitory effect was mediated by elevated intracellular cAMP and show here that analogs of cAMP, 8-bromoadenosine 3',5'-cyclic monophosphothioate and the Sp isomer of adenosine 3',5'-cyclic monophosphothioate, mimicked the CGRP suppressive effect on IL-1beta-induced ROS formation, NF-kappaB activation, and MCP-1 secretion. Thus increased endogenous CGRP secretion in lung inflammatory disease might eliminate the excessive response by elevating the cAMP level through inhibiting the ROS-NF-kappaB-MCP-1 pathway.

Autocrine Communication↗
PubMed2006

Fractionation of dissolved organic matter in mature landfill leachate and its recycling by ultrafiltration and evaporation combined processes.

XAD resin procedure was used to isolate dissolved organic matter (DOM) of a mature leachate collected from a municipal solid waste landfill in Beijing, China. The fulvic acids fraction dominated in collected leachate, accounting for 64% of DOM as dissolved organic carbon (DOC), and a high concentration of humic substances (HS) with a value of 441 mg l(-1) was found in the leachate. Molecular size distribution of DOM was also done by using batch ultrafiltration (UF) technique. Two major parts of the molecules of DOM were distributed in the regions of smaller than 1 kDa and 1-3.5 kDa, containing 45% and 43% of DOM as DOC, respectively. The laboratory-scale experiments were conducted to investigate and to develop an overall concept for mature leachate recycling based on UF and evaporation combined processes. Separation factor (SF) was applied to evaluate separation efficiency of UF. The data indicate that SF is strongly correlated with concentration factor. Second retentate from two-stage UF contained relatively high amount of DOM comprising 91% of HS and an insignificant concentration of heavy metals. The SF value for two-stage UF was more than 10. These results demonstrate that two-stage UF could effectively separate and refine HS in mature leachate from inorganic components. For achieving the main requirements as a fertilizer product, second retentate was further concentrated by evaporation, and contents of organic matter and dry-solids were obtained 13 wt.% and 25 wt.%, respectively. This study confirmed the feasibility of recycling HS from mature leachate.

Membranes, Artificial↗
PubMed2006

Aminoglycoside-induced and non-syndromic hearing loss is associated with the G7444A mutation in the mitochondrial COI/tRNASer(UCN) genes in two Chinese families.

We report here the clinical, genetic, and molecular characterization of two Chinese families with aminoglycoside induced and non-syndromic hearing impairment. Clinical and genetic evaluations revealed the variable severity and age-of-onset in hearing impairment in these families. Strikingly, there were extremely low penetrances of hearing impairment in these Chinese families. Sequence analysis of the complete mitochondrial genomes in these pedigrees showed the distinct sets of mtDNA polymorphism, in addition to the identical G7444A mutation associated with hearing loss. Indeed, the G7444A mutation in the CO1 gene and the precursor of tRNASer(UCN) gene is present in homoplasmy only in the maternal lineage of those pedigrees but not other members of these families and 164 Chinese controls. Their mitochondrial genomes belong to the Eastern Asian haplogroups C5a and D4a, respectively. In fact, the occurrence of the G7444A mutation in these several genetically unrelated subjects affected by hearing impairment strongly indicates that this mutation is involved in the pathogenesis of hearing impairment. However, there was the absence of other functionally significant mtDNA mutations in two Chinese pedigrees carrying the G7444A mutation. Therefore, nuclear modifier gene(s) or aminoglycoside(s) may play a role in the phenotypic expression of the deafness-associated G7444A mutation in these Chinese pedigrees.

Adolescent↗
PubMed2006

Classifications of ovarian cancer tissues by proteomic patterns.

Ovarian cancer is a morphologically and biologically heterogeneous disease. The identification of type-specific protein markers for ovarian cancer would provide the basis for more tailored treatments, as well as clues for understanding the molecular mechanisms governing cancer progression. In the present study, we used a novel approach to classify 24 ovarian cancer tissue samples based on the proteomic pattern of each sample. The method involved fractionation according to pI using chromatofocusing with analytical columns in the first dimension followed by separation of the proteins in each pI fraction using nonporous RP HPLC, which was coupled to an ESI-TOF mass analyzer for molecular weight (MW) analysis. A 2-D mass map of the protein content of each type of ovarian cancer tissue samples based upon pI versus intact protein MW was generated. Using this method, the clear cell and serous ovarian carcinoma samples were histologically distinguished by principal component analysis and clustering analysis based on their protein expression profiles and subtype-specific biomarker candidates of ovarian cancers were identified, which could be further investigated for future clinical study.

Adenocarcinoma, Clear Cell↗