1.Clinical Characteristics of Invasive Pulmonary Aspergillosis
Ning SHANG ; Jie CHANG ; Yingna LIU ; Xinping YUAN
Chinese Journal of Nosocomiology 1994;0(04):-
OBJECTIVE To study the clinical characteristics of invasive pulmonary aspergillosis(IPA).METHODS Based on the clinical data from 14 IPA cases identified by pathologic examination in the 454th Hospital,the characteristics of IPA were discussed,including the underlying diseases,symptoms,X-ray,CT,the treatment methods and the curative effect.The related literatures were also reviewed.RESULTS All of the 14 patients had underlying diseases.From them 5 were with pulmonary cancer(35.7%),3 with chronic obstructive pulmonary disease(21.4%),2 with pulmonary abscess(14.3%),2 were after chemotherapy for leukemia(14.3%),1 with pulmonary tuberculosis(7.1%)and 1 with diabetes(7.1%).The common symptoms of the 14 cases were febricity,productive cough and hemoptysis.Some of them also suffered with short of breath,night sweat,fatigue,chest pain and losing weight.The air crescent sign showed on X-ray and CT.Soft tissue masses with halo-sign on the margin,dense shadow of small masses within the alveoli,and multi-nodular shadows were also observed.Among 10 patients treated by antifungal medications,only 4 treated otherwise with operation were cured,4 patients died,and 2 patients did not complete the treatment scheme.CONCLUSIONS The patients with immunodeficiency are susceptible to IPA.The clinical manifestations of IPA are non-specific.The final diagnosis depends on the pathologic examination.The only medication is not sufficient for IPA patients.Pulmonary resection should be considered if the prolonged illness or frequent hemoptysis exist.
2.Effects of luteolin on CaM-CaMPK signaling pathway in hippocampus in epileptic rats
Junli ZHEN ; Yingna CHANG ; Tao FU ; Zhenzhen QU ; Jianqun LIU ; Weiping WANG
International Journal of Traditional Chinese Medicine 2016;38(3):232-237
Objective To explore the effects of luteolin on cognition function in pentylenetetrazol (PTZ)-induced epileptic rats and related mechanism.Methods Fifty male SD rats were randomly divided into a normal control group(n=8), a model group(n=12), and groups of 25, 50 mg/kg luteolin(both ofn=11), as well as 100 mg/kg luteolin group(n=8). Those rats were given different doses of luteolin (25, 50 and 100 mg/kg, daily, intragastric administration) for 36 consecutive days. Similarly, rats of the normal control group and the model group were given 0.5% sodium carboxymethyl cellulose suspension liquid via intragastric administration. Thirty minutes later, a model of epilepsy was induced using PTZ (40 mg/kg, daily) via intraperitoneal injection except the control group. Learning and memory of rats were evaluated by Morris water maze and novel objective recognition trials(including escape latency and recognition index). The levels of CaM and CaMPK were determined by ELISA methods, and expression of Ras proteins in the hippocampus were detected by Western Blot.Results Compared with the model group, luteolin treatment groups significantly shorten the escape latency(28.51 ± 3.84 s, 19.77 ± 5.41 s, 14.86 ± 2.76 svs. 37.08 ± 5.18 s) in the Morris water maze, and increased recognition index(18.77% ± 2.02%, 25.06% ± 4.32%, 31.92% ± 2.65%vs. 13.87% ± 2.14%) in the novel objection trial(P<0.05 orP<0.01). Meanwhile, CaM(140.33 ± 13.52 ng/L, 124.26 ± 9.97 ng/L, 113.52 ± 11.57 ng/Lvs. 158.36 ± 10.68 ng/L) and CaMPK(8.25 ± 1.37 ng/ml, 7.69 ± 0.84 ng/ml, 6.74 ± 0.93 ng/mlvs. 9.87 ± 1.02 ng/ml) were significantly decreased(P<0.05 orP<0.01). What’s more, the expression of Ras proteins(0.99 ± 0.08, 0.76 ± 0.07, 0.52 ± 0.07vs. 1.58 ± 0.12) was obviously decreased compared with the model group(P<0.05 orP<0.01).Conclusion Luteolin could effectively improve the cognition dysfunction of epileptic rats, and the mechanism might be relevant to regulate the CaM-CaMPK signaling pathway via down-regulation of CaM, CaMPK, as well as Ras protein.
3.Accidental discovery of copy number variation on chromosome 1 in a fetus with high risk of trisomy 13 suggested by NIPT.
Jiazhen CHANG ; Yingna SONG ; Qingwei QI ; Na HAO ; Juntao LIU
Chinese Journal of Medical Genetics 2023;40(8):922-927
OBJECTIVE:
To validate a fetus with high risk for trisomy 13 suggested by non-invasive prenatal testing (NIPT).
METHODS:
The fetus was selected as the study subject after the NIPT detection at Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences on February 18, 2019. Clinical data of the pregnant woman was collected. Fluorescence in situ hybridization (FISH), chromosomal karyotyping analysis and chromosomal microarray analysis (CMA) were carried out on amniotic fluid and umbilical cord blood and the couple's peripheral blood samples. Copy number variation sequencing (CNV-seq) was also performed on the placental and amniotic fluid samples following induced labor.
RESULTS:
The pregnant woman, a 38-year-old G4P1 gravida, was found to have abnormal fetal development by prenatal ultrasonography. NIPT test suggested that the fetus has a high risk for trisomy 13. Chromosomal karyotyping analysis of fetal amniotic fluid and umbilical cord blood were 46,XN,add(13)(p10). The result of CMA was arr[hg19]1q41q44(223937972_249224684)×3, with the size of the repeat fragment being approximately 25.29 Mb, the fetal karyotype was thereby revised as 46,XN,der(13)t(1;13)(q41;p10). Chromosomal karyotyping analysis and CMA of the parents' peripheral blood samples showed no obvious abnormality. The CNV-seq analysis of induced placenta revealed mosaicisms of normal karyotype and trisomy 13. The CNV-seq test of induced amniotic fluid confirmed a duplication of chr1:22446001_249220000 region spanning approximately 24.75 Mb, which was in keeping with the CMA results of amniotic fluid and umbilical cord blood samples.
CONCLUSION
NIPT may yield false positive result due to placenta mosaicism. Invasive prenatal diagnosis should be recommended to women with a high risk by NIPT test. And analysis of placenta can explain the inconsistency between the results of NIPT and invasive prenatal diagnosis.
Humans
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Female
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Pregnancy
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Trisomy 13 Syndrome/genetics*
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DNA Copy Number Variations
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Placenta
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Chromosomes, Human, Pair 1
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In Situ Hybridization, Fluorescence
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Prenatal Diagnosis/methods*
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Fetus
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Amniotic Fluid
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Chromosome Aberrations
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Trisomy/genetics*