8 research outputs found

    Data_Sheet_1_The effectiveness and safety of acupuncture for chemotherapy-induced peripheral neuropathy: A systematic review and meta-analysis.docx

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    ObjectivesThis systematic review and meta-analysis aimed to evaluate the effectiveness and safety of acupuncture on chemotherapy-induced peripheral neuropathy (CIPN).MethodsWe searched for relevant randomized controlled trials (RCTs) in PubMed, Cochrane Library, and Embase databases from their inception to 1 April 2022. The Functional Assessment of Cancer Therapy/Gynecologic Oncology Group-Neurotoxicity (FACT/GOG-Ntx), Brief Pain Inventory-Short Form (BPI-SF), the European Organisation for Research and Treatment of Cancer Quality of Life Questionnaire-Core30 (EORTC QLQ-C30), Numerical Rating Scale (NRS), and adverse events were the outcome measures. All studies had at least one of these outcome measures. Mean differences (MDs) with 95% confidence intervals (CIs) were assessed in the meta-analysis using the RevMan 5.3 software.ResultsFive studies were included in the analysis. The results showed that acupuncture and placebo acupuncture were not significantly different in reducing chemotherapy-induced neurotoxicity and functional disability (random-effects estimates; MD: 4.30; 95% CI: −0.85~9.45; P = 0.10; I2 = 74%). Acupuncture was better than placebo acupuncture in reducing pain severity and pain interference with patients' daily function (fixed-effect estimates; MD: −1.14; 95% CI: 1.87 to −0.42; P = 0.002; I2 = 13%). Acupuncture was not significantly different from placebo acupuncture in relieving CIPN symptoms (MD: −0.81; 95% CI: −2.02 to 0.40, P = 0.19). Acupuncture improved quality of life better than placebo acupuncture (MD: 10.10; 95% CI: 12.34 to 17.86, P = 0.01). No severe adverse events were recorded in all five studies.ConclusionThis meta-analysis suggests that acupuncture may be more effective and safer in reducing pain severity and pain interference with patients' daily function than placebo acupuncture. Additionally, acupuncture may improve the quality of life of patients with CIPN. However, large sample size studies are needed to confirm this conclusion.Systematic review registrationhttps://www.crd.york.ac.uk/prospero/display_record.php?RecordID=324930, identifier: CRD42022324930.</p

    Cep120 is required for centriole duplication and ciliogenesis.

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    <p>Wild type and <i>Cep120<sup>-/-</sup></i> pMEFs were coimmunostained for the indicated proteins. Most Cep120 mutant cells lacked either one or both centrioles, as indicated by γ ˜tubulin staining. Staining for Cep164, Ta3, and Odf2 showed that the missing centriole was the mother centriole. Staining for Arl13b and acetylated α ˜tubulin indicated no cilia being formed in Cep120 mutant cells. Arrowheads point to the staining of γ ˜tubulin (a centriole marker), the indicated proteins, or cilia.</p

    Ta3 interacts with Cep120 in the cell. FLAG-Cep120 was coexpressed with Ta3 (A) or various Ta3 mutants (B, C) in HEK293 cells as indicated.

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    <p>The protein lysates made from the cells were subjected to immunoblot (IB) or immunoprecipitation (IP) followed by immunoblot with the indicated antibodies. Note that the interaction of Cep120 with Ta3 requires the coil-coiled (CC) domain of Ta3 (B, C).</p

    Ta3 is required for asymmetrical localization of Cep120 to the daughter centriole.

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    <p>Wild type and <i>Ta3</i> mutant primary mouse embryonic fibroblasts (pMEFs) were coimmunostained for Cep120 and γ ˜tubulin (A) or Odf2 and Cep120 (B), together with DAPI (for nuclei). Arrowheads indicate the specific staining at centrioles. The Cep120 signal at the daughter and mother centrioles (DC and MC, respectively) was quantified for 21 randomly chosen cells, using NIH image J. Cep120 signal ratios were then calculated, specifically the DC to MC ratio and the wild type to Ta3 mutant ratio (average + standard deviation) (C). (D) No significant changes in Cep120 levels in <i>Ta3</i> mutant MEFs. Immunoblots show the expression of endogenous Ta3 and Cep120 in wild type and <i>Ta3</i> mutant MEFs, with tubulin as a loading control.</p

    Loss of Cep120 results in early embryonic lethality, hydrocephalus, and cerebellar hypoplasia in mice.

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    <p>(A) The gene targeting strategy used to create mouse <i>Cep120<sup>-</sup></i> and <i>Cep120<sup>f</sup></i> mutant alleles. Open rectangles refer to exons (which are numbered), lines to introns, grey rectangles to Frt sites, and triangles to loxP sites. BglII (Bg) restriction sites and a probe for Southern blot are indicated. Neo, neomycin gene; DTA, diphtheria toxin A gene. (B) Southern blot analysis shows a representative mutant and wild type (wt) ES cell clones. (C) Lateral view of wild type and <i>Cep120<sup>-/-</sup></i> embryos. Note that the development of Cep120 mutant embryos is delayed and the heart loops in the opposite direction (indicated by the arrow). (D–G) Morphology of two-week-old (P14) unskinned mouse heads (D), brains (E, F), and cerebellums (G), with indicated genotypes. The lines are in the same length for both wt and mutant, thus indicating the relative brain size or the extent of hydrocephalus in the mutant. Hematoxylin and eosin (H&E) staining of sagittal brain sections (E) confirms that the mutant ventricles of the brain are severely dilated. The boxed area in F is enlarged in (G). Cerebellums are outlined. The mutant cerebellum is significantly smaller (F).</p

    Loss of Cep120 results in failed expansion of granule neuron progenitors (GNPs), due to lack of a response to Hedgehog signaling.

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    <p>(A–F) Sagittal sections of P1, P7, and P14 wild type and mutant cerebellums were coimmunostained for Pax6 (red), Calb1 (green), and nuclei (DAPI, blue). Pax6 and Calb1 label GNPs and Purkinje cells, respectively. Framed areas in panels A–F are enlarged in A′–F′. EGL, external granule cell layer; PCL, Purkinje cell layer; ML, molecular layer; IGL, inner granule layer. Genotypes are shown to the left. (G–H) LacZ staining of the P7 cerebellum is positive in wild type animals (G), but negative in the Cep120 mutant (H). Genotypes are indicated on both sides. Cerebellums are outlined, and cerebellar posterior lobes are indicated by asterisks.</p

    The Cep120 mutation results in cerebellar hypoplasia.

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    <p>Sagittal sections of P1, P7, and P14 wild type and <i>Cep120<sup>f/-</sup></i>; <i>nes-Cre</i> mutant cerebellums were stained with cresyl violet. Framed areas are enlarged in the corresponding lower panels. EGL, external granule cell layer; PCL, Purkinje cell layer; ML, molecular layer; and IGL, inner granule layer.</p

    Failed centriole duplication, maturation, and ciliogenesis in cerebellar granule neuron progenitors (CGNPs) and ependymal cells in the Cep120 mutant.

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    <p>(A–D) Sagittal brain sections of P14 mice with the indicated genotypes were coimmunostained for acetylated α ˜tubulin and Arl13b, cilia markers. The fourth ventricular choroid plexus is circled. Framed areas in panels A and B are enlarged in A′/A″ and B′/B″. Panels A″ and B″ show representative areas of ependyma near the fourth ventricle. Panels C and D show representative areas of CGNPs. Arrowheads indicate representative cilia. Note that cilia develop in the <i>Cep120<sup>f/-</sup></i>; <i>nes-Cre</i> choroid plexus, but not in ependymal cells and CGNPs. (G–L) Sagittal cerebellar sections of P14 mice with the indicated genotypes were coimmunostained for γ ˜tubulin and Cep120, Odf2, or Ta3, as shown. Note that very few centrioles are present in <i>Cep120<sup>f/-</sup></i>; <i>nes-Cre</i> CGNPs, relative to wild type CGNPs. Arrowheads indicate one or two representative centrioles in each panel.</p
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