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Pediatric acute myeloid leukemia patients with i(17)(q10) mimicking acute promyelocytic leukemia: Two case reports

2022-06-28 05:59:38HongXiaYanWeiHuaZhangJinQuanWenYanHeLiuBaoJuanZhangDuoJi
World Journal of Clinical Cases 2022年16期
關(guān)鍵詞:貨位齒輪箱生長(zhǎng)

INTRODUCTION

Chromosome i(17)(q10) abnormality is described as any unreasonable damage or breakage of the centromeres of chromosome 17, resulting in absence of the short arm and an iso-arm of the long arm[1]. Isochromosome 17 i(17)(q10) is mainly associated with chronic myeloid leukemia (CML)[2,3], myelodysplastic syndrome/myeloproliferative tumors (MDS/MPD)[4-6], and acute myeloid leukemia (AML)[6,7]. Genetic mutation analysis showed that 95% of patients with chromosome karyotype i(17)(q10) carried at least one mutation, and on average three mutations. The three most commonly mutated genes were(66%),(65%), and(48%)[8,9]. In acute promyelocytic leukemia (APL), chromosome karyotype i(17)(q10) was often accompanied by t(15;17) and PML-RARa fusion gene with an incidence of 1.9% and 4.1%, respectively[10,11]. APL children with i(17)(q10) have poor prognosis[12]. In a group study of 478 children with AML, chromosome karyotype analysis showed only one i(17)(q10) abnormality case, without morphological description and prognostic evaluation[13]. A 10-year-old African Black APL child carrying i(17)(q10) karyotype but without t(15;17) abnormality, who was in serious condition at admission, did not get tumor remission after treatment, and died within 2 wk[14]. A Chinese i(17)(q10) AML adult with a similar phenotype to APL was reported[15]. In the present case study, we treated 1 AML child with i(17)(q10) and 1 AML child with i(17)(q10) and (14)(p11) who had a phenotype similar to APL in our department. These two cases were investigated and followed up, and their clinical significance was discussed.

CASE PRESENTATION

Chief complaints

A 3-year-old boy of Han nationality, was admitted to the Pediatric Hematology Department of Xianyang Caihong Hospital, China on December 19, 2016. The boy had paleness and fever for more than half a month, as well as exophthalmos and pain in the right knee joint due to unknown reasons for two weeks.

露地栽植時(shí),一般株行距為30×40cm,施入腐熟的有機(jī)肥,并施入過(guò)磷酸鈣和草木灰等含磷鉀成分高的肥料作基肥,栽植后將根莖壓緊,栽植后需澆透水。溪蓀鳶尾的生長(zhǎng)旺盛期為6-8月,持續(xù)時(shí)間約為3個(gè)月,生長(zhǎng)迅速,根系發(fā)達(dá),形成了較完整的營(yíng)養(yǎng)器官。生長(zhǎng)旺盛期可追肥2次,每畝可追施尿素10-15kg、磷酸二銨5-10kg[3]。栽植后及時(shí)中耕除草,清除雜草時(shí)勿傷根系,根據(jù)地面情況一般每周澆水1次,保證正常生長(zhǎng)。夏季地表的高溫高熱會(huì)灼傷苗木,可每周澆水2次,早晚進(jìn)行適量噴水。生長(zhǎng)后期從10月上旬至11月初,苗生長(zhǎng)快速下降。期間適當(dāng)少灌,每周澆水1次。做好植株安全越冬的工作,初冬澆1次封凍水。

1.校園環(huán)境方面。好的環(huán)境對(duì)于學(xué)生的學(xué)習(xí)與成長(zhǎng)有著積極作用。為使學(xué)生更好地接受傳統(tǒng)文化,主動(dòng)誦讀經(jīng)典詩(shī)文,學(xué)校方面應(yīng)加強(qiáng)校園文化建設(shè)。譬如在文化墻上手繪《弟子規(guī)》或者是《三字經(jīng)》篇章,使其成為學(xué)生的行為準(zhǔn)則:孝敬父母、尊師重道、團(tuán)結(jié)友愛(ài)、積極進(jìn)取。教學(xué)樓走廊墻壁上應(yīng)掛詩(shī)詞名作,學(xué)校的廣播站應(yīng)定期定時(shí)播放經(jīng)典古詩(shī)文;在班級(jí)文化建設(shè)方面也應(yīng)注重經(jīng)典誦讀,班級(jí)中學(xué)習(xí)園地應(yīng)不定時(shí)展示出學(xué)生關(guān)于經(jīng)典詩(shī)文的繪畫(huà)、寫(xiě)作及摘錄作品等。通過(guò)校園文化的建設(shè),使整個(gè)校園充滿詩(shī)意,促進(jìn)學(xué)生對(duì)古詩(shī)文的學(xué)習(xí)。

A 12-year-old Han boy was admitted to our hospital with a history of a pale complexion for one month and skin bleeding for 10 d.

He had a fever of 38.2 °C, moderate anemia, scattered red bleeding spots on the skin, protruded eyeballs, and no swelling of the superficial lymph nodes.Initial blood tests showed the following: Hb 75 g/L, white blood cell (WBC) count 5.82 × 10/L, and platelet (PLT) count 73 × 10/L.

History of present illness

當(dāng)入庫(kù)貨物i目標(biāo)貨位與出庫(kù)貨物n所在貨位同層,入庫(kù)貨物j目標(biāo)貨位與出庫(kù)貨物m所在貨位同層(yi=yn≠yj=ym)時(shí),

He had moderate anemia and bleeding spots on the skin and mucosa throughout the body. Initial blood test results showed the following: Hb 68 g/L, WBC count 17.53 × 10/L, and PLT count 60 × 10/L.

History of past illness

Bone marrow smear: Case 1 showed active bone marrow with nucleated cell hyperplasia. Case 2 originally had granulocyte at 1.0%, and abnormal early young granulocyte at 83.0% and 85.0%, respectively. The cytoplasm was bulky and filled with azure particles. Plasma particles were visible both inside and outside some cells, with less outside the cells. Round or oval nucleus, coarse chromatin, and indistinct nucleoli were observed. Acute promyelocytic leukemia is shown in Figure 1.

For case 2, the following mutation sites might be associated with the disease: (1) TAL1 (T-Cell Acute Lymphocytic Leukemia genemutation (NM_003189:exon6:c.821_822insGGGGGGGGGGGGGG:p.G274fs), with a mutation frequency of 44.2%; (2) TTN mutation in the titin gene (NM_001267550:exon96:c.C27746T:p.T9249M), with a mutation frequency of 53.5%; (3) PHLPP1 (PH Domain And Leucine Rich Repeat Protein Phospatase1) gene mutation (NM_19449:exon1: c.77_78insTCTGG:pA26fs), with a mutation frequency of 35.3%; (4) OR5B12 (Olfactory Receptor Family 5 Subfamily B Member 12) gene mutation (NM_001004733:exon1:c.597delT:p.199fs), with a mutation frequency of 83.5%; (5) DDX11 (DEAD/H-BOX Helicase 11) genemutation (NM_152438: exon7:c.G778A:p.R263Q), with a mutation frequency of 18.8%.

Personal and family history

He had been in good health condition, with no family history of inherited blood disorder, no history of tumor-associated genetic abnormalities, and no history of drug or food allergies.

There is no personal and family history.

Physical examination

Upon examination, he had a fever of 38.2 °C, moderate anemia, scattered red bleeding spots on the skin, protruded eyeballs, and no swelling of the superficial lymph nodes. On auscultation, his heart and lung were normal, and the liver and spleen were not examined.

He had moderate anemia and bleeding spots on the skin and mucosa throughout the body. Auscultation of the heart and lung showed no abnormalities. Subcostal areas of the liver and spleen were not examined.

Laboratory examinations

A volume of 0.1 mL bone marrow fluid was extracted from the posterior superior iliac spine (sampling was very difficult), a bone marrow smear was prepared and submitted for examination. Chromosome G-banding karyotype analysis: 3 mL of sterile bone marrow fluid was taken from the patient, and gbanding technique was employed to detect the chromosomes in trypsin-digested short-term cell culture. Karyotype results were analyzed according to the international system for human cytogenetic nomenclature (ISCN, 1991).

We thank the Hematological Tumor Molecular Special Detection Technology Research Center of Kindstar Global (Wuhan) for its technological support.

PML-RARa fusion gene was detected by real-time quantitative PCR: A volume of 2 mL bone marrow fluid with heparin anticoagulant was collected to isolate the mononuclear cells, and total DNA of mononuclear cells was extracted.

Imaging examinations

The following results were revealed: Case 1: 46XY, i(17)(q10)[9]/46, XY[11], long equi arm of chromosome 17; Cases 2: 46XY, Add(14)(P11), i(17)(q10)[4]/46, XY[1], a short arm of chromosome 14 with an additional fragment of unknown origin and a long arm of chromosome 17, as shown in Figure 2.

FINAL DIAGNOSIS

Acute promyelocytic leukemia -like acute myeloid leukemia with i(17)(q10).

TREATMENT

Phase Ⅰ: Two children were treated with ATAR combined with ATO to induce remission: ATAR (30 mg/M2/d), divided 3 times, orally, D1-30; ATO (0.02 mg/Kg), 1 time/day, intravenous infusion, D1-28. Then they were treated with low molecular weight heparin anticoagulant correction therapy based on the coagulation test. Bone marrow cell morphology and leukocyte residual lesions were detected on D29. Blood WBC count was 27.53 × 10/L. Considering the possibility of retinoic acid syndrome, dexamethasone tablets were administered orally at 1.5 mg/time, 3 times a day. With fever regression, WBC was reduced to 12.27 × 10/L on D7. Case 2 showed fever on D2 of treatment, with a temperature of 38.5 ℃, and still had a fever on D3. Blood routine test showed a WBC count of 27.53 × 10/L. Considering the possibility of the retinoic acid syndrome, dexamethasone tablet was taken 1.5 mg/time, 3 times a day. With fever regression, WBC decreased to 12.27 × 10/L in D7.

Phase Ⅱ: On D33, case 1 was treated with the DAE regimen, which including the following: DNR (40 mg/M2/d), D1, 3 and 5, intravenous infusion, once a day; Ara-c (200mg/M2/d), D 1-7, q12h, subcutaneous injection; and Vp-16 /E (100mg/M2/d), D 5, 6, 7, intravenous infusion, once a day. Reexamination of bone marrow cell morphology on D 65 showed no remission. The pediatric patient gave up treatment and discharged themselves. On D154, he came to the hospital again with fatigue, sallow complexion, skin hemorrhagic spots, bone pain, and eyeball herniation. Bone marrow examination showed 85% abnormal promyelocytic granulocytes. D156 Chemotherapy with MAH protocol: M (10 mg/M2/d), D1, 2 and 3; A (200 mg/M2/d), D1-7, q12h, subcutaneous injection; and H (3 mg/M2/d),D 1-7, subcutaneous injection. Case 2 was treated with the MAH regimen on D 47 and D80. The doses and methods were as above. On D115, he was treated with IDA (10mg/M2/ D1-3); intravenous infusion; once a day. The dosage and usage of the ara-C and H were the same as before. On D145, bone marrow cell morphology was evaluated, residual lesions were detected by flow cytometry, and WT1 gene copy number was detected by molecular biological techniques (See Methods). On D175, he was treated with HD ara-C (2.0 g/M2/d); D1, 3, 5 and 7; q12h. The dose and usage of HD ara-C were the same as above. On D205, HD ara-C dose and usage were the same as above: Vp-16 (100 mg/M2/d), D1-5; intravenous infusion. On D 235, he received HD ara-C (3.0g/M2/d); D1, 3, 5, 7; q12h; the dose and usage were the same as above. During D265-730, 6-MP [50 mg/M2/d (D1-21)] plus low-dose ara-C (40mg/M2) were given. D1-4 (D22-28) maintenance therapy: Bone marrow cell morphology was returned one year after drug discontinuation, residual lesions were detected using flow cytometry, and WT1 gene copy number was detected by molecular biological tools (See methods).

OUTCOME AND FOLLOW-UP

There is no history of past illness.

Karyotype analysis

There is no imaging examinations.

Fully-instrumented submersible housing detection

Case 1: The nuclear in situ hybridization (nuc ish) (PML × 2, RARA × 3) (180/400) showed no fusion signal by PML/RARA translocation probe, and the copy number of RARA (located at 17q21) site increased, accounting for about 45%.

Case 2: The nuc ish (PML × 2, RARA × 2) showed no abnormal signal in the PML/RARA locus, and the detection result was negative as shown in Figure 3.

Immune typing

Abnormal cells were accounted for 88% in Case 1 and 78% in Case 2. Flow cytometric analysis on CD45/SSC dot plot showed that CD9, CD13, CD33, and CD38 were mainly expressed in all analyses, while CD64, CD123, and MPO were only expressed in some analyses. CD58 was expressed in case 1 and CD15 was expressed in case 2, as shown in Figure 4. Molecular biological detection: PML/RARa, PLZF/RARa, NPM/RARa, STAT5b/RARa, NuMA1/RARa, PRKARIA/RARa, and FIPIL1/RARa fusion-gene tests showed negative results.

Detection of gene (exon) variation related to myeloid and gonorrhea hematologic malignancies was performed by targeted capture method. Mutation sites were clearly associated with the disease, and all of them had mutations of WT1 (Wilms Tumor 11). Case 1 WT1: NM_024426: exon9:c.G1367C:p.C456s; mutation frequency 49.2%. Case 2 WT1: NM_024426:exon1:c.410_413del:p.137_138del; mutation frequency 100%. Case 1 with EP300 (E1A Binding Protein p300) mutations: NM_001429: exon31:c.C5449T:p.Q1817X; mutation frequency 72.1%.

在經(jīng)歷了這樣特殊的課程之后,從新加坡中學(xué)走出來(lái)的學(xué)生具有非常敏銳的“批判性思維”和“辯證思維”,他們的邏輯思維能力快速成長(zhǎng),也同樣對(duì)于他們的學(xué)術(shù)課程大有助益。

For case 1, the following mutation sites might be associated with the disease: (1) USP6 (NM_004505:exon12:c.854delG:p.W285fs) was a frameshift mutation, with a mutation frequency of 32.6%; (2) NUTM2G (NM_001170741:exon7:c.C2102T:p.701L) was a missense mutation, with a mutation frequency of 78.8%.

He was diagnosed with APL 3 years ago in a local hospital based on bone marrow morphology and immunological classification, with negative PML-RARa fusion gene at the time of diagnosis.The patient received all-trans retinoic acid (ARAT) and arsenic trioxide (ATO) as induction therapy, and bone marrow examination showed no tumor remission on D29. He then received three cycles of consolidation therapy (DA, HA, and MA regimen) and maintenance therapy, bone marrow evaluation showed complete remission, and the treatment was stopped.

綜上所述,隨著信息時(shí)代的到來(lái),為了跟上網(wǎng)絡(luò)發(fā)展的步伐,我們應(yīng)該提高新聞編輯的價(jià)值,根據(jù)實(shí)際情況強(qiáng)化信息的使用質(zhì)量,這對(duì)于新聞發(fā)展有著比較大的作用。而新聞播音主持作為公眾人物,應(yīng)該注意從自身做起,提高自身的語(yǔ)言表達(dá)能力,時(shí)刻記著自身的責(zé)任和義務(wù),在播報(bào)的過(guò)程中將自身的個(gè)性化技巧表現(xiàn)出來(lái),吸引人們的注意力,從而在一定程度上提高電視新聞的收視率,促進(jìn)電視新聞播音主持行業(yè)的發(fā)展。

由于風(fēng)力發(fā)電機(jī)組多安裝在高山、荒野、海島等風(fēng)口處,受無(wú)規(guī)律的變向變載荷的風(fēng)力作用以及強(qiáng)陣風(fēng)的沖擊,加之所處的自然環(huán)境交通不便,而且機(jī)組安裝在塔頂?shù)莫M小空間內(nèi),一旦出現(xiàn)故障,修復(fù)非常困難,故對(duì)其可靠性等提出了比一般機(jī)械高得多的要求。大量的實(shí)踐證明,整個(gè)機(jī)組的薄弱環(huán)節(jié)常常就是齒輪箱。因此,風(fēng)力發(fā)電機(jī)組齒輪箱在投入使用前,都會(huì)進(jìn)行嚴(yán)格的試驗(yàn),以確保其高可靠性。而測(cè)試齒輪箱的變頻電動(dòng)機(jī),必須經(jīng)受齒輪箱的各種復(fù)雜工況,這也就對(duì)電動(dòng)機(jī)提出了較高的要求。

Treatment outcome

Case 1 review of bone marrow on D29 and D65: It was still very difficult to collect bone marrow; myelodysplastic hyperplasia was pronounced; abnormal promyelocytic granulocytes were 33% and 78%, respectively; the treatment was ineffective on D156; MAH regimen was used for chemotherapy; the patient died of intracranial hemorrhage on D162.

1.2.5 評(píng)價(jià)標(biāo)準(zhǔn) ①對(duì)糖尿病知識(shí)的認(rèn)知≥60為合格。②綜合干預(yù)的效果評(píng)價(jià)包括飲食控制、運(yùn)動(dòng)和血糖、尿糖監(jiān)測(cè)。

在開(kāi)展高中政治課程的教學(xué)過(guò)程中,教師既能夠?qū)⑽⒄n運(yùn)用在實(shí)際的課堂教學(xué)過(guò)程中,同時(shí)也能夠使政治課堂向外拓展,在平時(shí)的生活中給予學(xué)生適當(dāng)?shù)妮o助與指導(dǎo),讓其可以學(xué)習(xí)到比較全面的政治教育知識(shí),將政治教育的作用與目的充分發(fā)揮出來(lái)。概括來(lái)講,教師應(yīng)該相應(yīng)地制作一些與高中政治課程教學(xué)重難點(diǎn)內(nèi)容相關(guān)的課件,引導(dǎo)學(xué)生在課下進(jìn)行深入學(xué)習(xí),尤其是就部分在課堂上未能切實(shí)掌握此部分內(nèi)容的學(xué)生而言,如果在課下得到教師正確的教學(xué)指導(dǎo),就可以系統(tǒng)性地了解相關(guān)知識(shí)內(nèi)容,從而不僅能夠進(jìn)一步提高學(xué)習(xí)效率,而且還能對(duì)他們的學(xué)習(xí)能力與學(xué)習(xí)興趣進(jìn)行培養(yǎng)。

Case 2 review of bone marrow on D29: It was still very difficult to obtain bone marrow samples; myelodysplasia decreased and promyelocytic granulocytes accounted for 32%. On repeated examination of bone marrow on D46, D145, D265 to D730, it was still very difficult to obtain bone marrow samples; reduced myelodysplasia was observed; abnormal morphology of promyelocytic granulocytes accounted for 2%; cytoplasm contained a large number of arrocysts; nuclei had lumps and no nucleolus. Residual leukemia detection revealed no immunophenotypic abnormal cell population (residual leukemia cells < 10); complete remission occurred. Up to now, the drug has been discontinued for 1 year, and the clinical, morphological, and flow cytometry results continued to show complete remission. However, the copy number of thegene was 1010-1087, and the expression rate was 51.95%-55.29%, which indicated the risk of recurrence, and allogeneic hematopoietic stem cell transplantation was necessary.

DISCUSSION

APL is a rare subtype of AML and has different morphological and immunological characteristics compared with other myeloid leukemia cells. Karyotype t (15;17) is a unique chromosome translocation in APL. At the molecular level, PML/RARα fusion gene is formed by translocation of PML gene at 15q and RARα gene at 17q.Therefore, it is a highly specific cytogenetic marker for this type of leukemia. In this case study, the phenotype of 2 children showed typical APL characteristics, especially some cells had inner and outer plasma membrane, with thick azinophilus granules (Figure 1). Immunophenotypic markers mainly included CD9, CD13, CD33, CD38 (Figure 2), and CD64, CD123, MPO were also expressed in case 1. In addition, case 1 also had the expression of CD15, which was consistent with the immunophenotype of APL[16,17] and the isolated i(17)(q10) AML with similar APL morphology.

Previously, 4 isolated i(17) (q10) cases were reported, including 2 children[13,14], 1 adult[15], 1 case without age information[18], and 3 cases with M3 (APL) FAB classification. There were no t(15;17) and PML-RARa fusion gene detected and patients had no responses to ATRA treatment[15]. One case did not respond to chemotherapy and the survival time was less than 1 mo[14]. The other 2 cases did not mention prognosis[13,19]. In this study, there were 2 cases examined, case 1 was isolated i(17)(q10), case 2 was isolated i(17)(q10) add(14)(p11). The t(15;17) was not present, and PML-RARa fusion gene was not detected by Fully-instrumented submersible housing and second-generation sequencing, which rendered ATRA and AsOcombined chemotherapy ineffective. Case 1 survived 5.5 mo. Case 2 achieved sustained complete remission after intensive chemotherapy with acute non-eluting regimen. The difference might not be related to isolated i(17)(q10) add(14)(P11), which was speculated to contribute to the transport of chemotherapeutic drugs. Similar studies have not been reported on leukemia patients, and the underlying specific mechanism needs further exploration. However, with the high expression ofgene, the risk of recurrence is still very high[20]. Further clinical follow-up is required, and hematopoietic stem cell transplantation is necessary. However, this case was different from occult APL and APL with i(17)(q10) and PML-RARa fusion gene, for which the ATRA and AsOcombined chemotherapy was effective[2,18].

Patients with myeloid tumor i(17)(q10) are mostly MDS/MPO+ patients with a chronic history, and often have pathological hematopoiesis in granulocyte, erythrocyte, and megakaryocyte lines, with an average of 3 gene mutations, mainly,, and[8,9]. In this study, 2 patients had a short course of the disease, with no history of MDS/MPO+, and no erythrocyte or megakaryocyte pathological hematopoiesis except granulocyte lineage, which was similar to a 27-year-old female APLlike AML patient with a short course of the disease, having no chronic history and multi-family pathological hematopoiesis[15].

Gene mutations in these APL-like AML cases were reported for the first time, and there were 5 mutations in case 1, including WT EP300 c.854delg: P w285fs frame-shift mutation and C.C2102T: P 701L missense mutation.,,, andmutations were found in case 2. Both cases hadgene mutations, which were consistent with the characteristics of i(17)(q10) gene mutations (0-6) in MDS/MPO+ patients, but the gene mutation points were completely different. Therefore, case with i(17)(q10) was clinically diagnosed. The morphological diversity was probably due to different mutation patterns, and the number and order of the mutations might play a key role[8]. Therefore, both morphologic and immunological manifestations of APL were found in 2 children without t(15;17) and PML-RARa fusion-gene expression. Though preliminary diagnosis of AML morphologically similar to APL[15] were made for both children, the treatment failed in case 1, and case 2 with add(14)(p11) achieved sustained complete remission after chemotherapy, which might be related to the different gene mutation points.

Through literature review, 6 patients with i(17)(q10) have been known (including 2 in this group), 5 morphologically similar to AML, 1 without FAB classification mentioned[13], 5 with isolated TYPE i(17)(q10), 1 with add(14)(p11), and 3 patients (including 2 in this group) had CD33 immunophenotype with CD3 MPO expression[15]. Using existing genetic and molecular biological techniques, t(15;17) among the 6 patients with PML-RARa fusion gene were not detected, 3 patients failed to respond toATRA-AsOand chemotherapy and died (survival shorter than 5.5 mo), 1 patient achieved sustained complete response after chemotherapy, and 2 patients did not show prognosis[13,18].

著作權(quán)法采取“以用設(shè)權(quán)”的方式意味著,如果法律賦予作者控制某種作品使用行為,那么第三人實(shí)施這一行為時(shí),需獲得權(quán)利人的授權(quán)許可。換言之,權(quán)利人控制作品使用行為,也就有權(quán)從第三人使用作品的行為中獲益。然而,作品使用行為是難以完全列舉的,對(duì)于一些作品使用行為未被法律定性化為有名權(quán)利,而立法又未明確否定的利益,該如何保護(hù)?對(duì)此,各國(guó)有不同的做法。

Morphology, immunology, chromosomal karyotype, and molecular biological genotyping of 6 cases with i(17)(q10) in different periods and their prognosis are shown in Table 1.

CONCLUSION

APL-like AML with i(17)(q10) has morphological and immunological characteristics similar to APL, without t(15;17) and PML-RARa fusion gene expression. ATRA-AsOand chemotherapy were not effective in treating the patients, with short survival period. If a chromosomal addition occurred, a sustained complete remission should be achieved and related clinical manifestations should be revealed. It is necessary to further strengthen the molecular biological study and collect a large number of cases to provide better treatment strategies.

ACKNOWLEDGEMENTS

Immunophenotype: 2 mL of bone marrow fluid with heparin anticoagulant was obtained, 5x10-5×10/mL cells were isolated using FACSort flow cytometry (BD Biosciences) and analyzed with CellQuest software > The expression levels of leukemia related antigens in the cell population were analyzed and calculated. Monoclonal antibodies used included HLA-DR, CD2, CD3, CD4, CD7, CD8, CD9, CD11b, CD13, CD14, CD15, CD16, CD19, CD22, CD33, and CD34 Labeled by FITC, PE, and PerCP, or APC- CD38, CD56, CD64, CD71, CD117, CD123, and MPO. All antibodies were purchased from BD Biosciences.

(3)施工重點(diǎn)環(huán)節(jié)不精準(zhǔn)。如驗(yàn)收開(kāi)鉆、定點(diǎn)測(cè)斜,進(jìn)入沙河街等特殊地層、水平井使用地質(zhì)導(dǎo)向儀器、電測(cè)、下套管、固井等特殊環(huán)節(jié),井隊(duì)一直以原有的施工方式方法實(shí)施,缺乏精準(zhǔn)性。

FOOTNOTES

Yan HX and Wen JQ contributed to conception and design of the study; Yan HX and Zhang WH are the co-first author; Zhang WH organized the database; Yan HX wrote the first draft of the manuscript; all authors contributed to manuscript revision, read, and approved the submitted version.

Shaanxi Natural Science Foundation, No. 2020SF-004.

Consent was obtained from relatives of the patient for publication of this report and any accompanying images.

The authors declare that they have no conflicts of interest.

為酒店客人提供的入住引導(dǎo)服務(wù)是通過(guò)在酒店里面布置引導(dǎo)牌來(lái)實(shí)現(xiàn)的。根據(jù)客人所持的標(biāo)識(shí)卡,并經(jīng)過(guò)樓底系統(tǒng)、PMS系統(tǒng)、電子牌控制系統(tǒng)、感知系統(tǒng)等對(duì)客人進(jìn)行一步步的引導(dǎo),讓客人可以在結(jié)構(gòu)復(fù)雜的酒店中迅速、方便地找到自己的房間。所有入住酒店的客人都可以享受到入住引導(dǎo)服務(wù)。

The authors have read the CARE Checklist (2016), and the manuscript was prepared and revised according to the CARE Checklist (2016).

This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BYNC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is noncommercial. See: https://creativecommons.org/Licenses/by-nc/4.0/

China

Hong-Xia Yan 0000-0002-1722-716X; Wei-Hua Zhang 0000-0002-4579-3492; Jin-Quan Wen 0000-0001-9202-6598; Yan-He Liu 0000-0001-5141-8122; Bao-Juan Zhang 0000-0002-1534-9622; A-Duo Ji 0000-0001-6328-6227.

Xing YX

A

但是,通過(guò)研究英語(yǔ)和漢語(yǔ)中人體詞的多義性,我們也發(fā)現(xiàn)英、漢兩種語(yǔ)言在人體詞的語(yǔ)義轉(zhuǎn)移方面有不少異同點(diǎn)。我們會(huì)不斷研究,將情感、文化等因素考慮在內(nèi),以期發(fā)現(xiàn)兩種語(yǔ)言人體詞意義構(gòu)建上的差異性。

Xing YX

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