1.Incidence of leukemia in infants in Shanxi Children's Hospital
Xinghong CHANG ; Xiaohuan WANG
Journal of Leukemia & Lymphoma 2017;26(3):181-182,192
Objective To investigate the incidence of leukemia in infants, and to understand the status of this disease in recent years. Methods A total of 5802 children aged median 6 years (0-12 years) with first time bone marrow biopsy from January 2009 to December 2015 were retrospectively analyzed, and the results of bone marrow image analysis were analyzed retrospectively to investigate the incidence of leukemia. Results Of the 5802 cases, 480 (8.27 %) cases were children with leukemia. Among them, 381 (79.38 %) cases were acute lymphocytic leukemia (ALL), 99 (20.62 %) cases were acute myeloid leukemia (AML). The proportion of children with leukemia with first time marrow puncture was 5.33%(40/750), 4.92%(36/731), 7.06%(58/821), 8.34%(78/935), 10.13%(88/868), 10.89%(92/845), and 10.33%(88/852) from 2009 to 2015, respectively. The proportion of male patients per year was more than female, and the incidence in preschool and school-age children was higher [33.75 % (162/480) and 34.79 % (167/480), respectively]. Conclusion The proportion of children's leukemia in children with the first time bone marrow aspiration in Shanxi Children's Hospital increases year by year, and its risk factors need to be further analyzed.
2.Disease constitution analysis of 4 590 children with abnormalities in the blood cells
Xinghong CHANG ; Guoping HAO ; Youcai FENG
Journal of Leukemia & Lymphoma 2015;24(12):743-745
Objective To investigate the significance of bone marrow cell morphology on clinical diagnosis of children hematopoietic diseases.Methods The data of bone marrow cell morphology in the bone marrow puncture specimens from 4 590 children admitted to Children' s Hospital of Shanxi Province from January 2009 to December 2014 were retrospectively analyzed.Results The proportion of infancy patients was the highest in 4 590 bone marrow specimens, accounting for 29.0 % (1 333/4 590), then that of the toddler age patients was second highest, accounting for 26.7 % (1 224/4 590).The constituent ratio of thrombocytopenic purpura (ITP) at the different ages was the highest.The most common diseases in bone marrow cell morphology diagnosis were in order of ITP, iron deficiency anemia (IDA), infectious bone marrow, leukemia (acute lymphoblastic leukemia, acute myeloid leukemia), aplastic anemia and so on.Conclusions Accurate analysis of bone marrow cell morphology is still the most basic and rapid approach in children with hematopoietic system disease, which has important value.Except hematopoietic system diseases, once fever of unknown origin, hepatosplenomegaly and enlargement of lymph nodes the patients should be early given bone marrow cell morphology check, early diagnosis and therapy.
3.Mechanism of Shengmai Injection Against Cerebral Ischemia Based on Proteomics
Jingtong LIU ; Shaowei HU ; Mengli CHANG ; Jing XU ; Qingqing CAI ; Xinghong LI ; Liying TANG ; Huanhuan WANG ; Hongwei WU
Chinese Journal of Experimental Traditional Medical Formulae 2025;31(9):57-67
ObjectiveTo evaluate pharmacological effects of Shengmai injection(SMI)on cerebral ischemia and study its neuroprotective mechanism. MethodsMale specific pathogen-free (SPF) Sprague-Dawley (SD) rats were randomly divided into a sham group, a model group, a low-dose SMI group(3 mL·kg-1), a middle-dose SMI group(6 mL·kg-1), a high-dose SMI group(12 mL·kg-1), and a Ginaton group(4 mL·kg-1)according to the random number table method, with 12 rats in each group. The rat model of cerebral ischemia-reperfusion(MCAO/R)was prepared via the suture method. The administration groups were intraperitoneally injected with corresponding concentrations of SMI or Ginaton injection after reperfusion, which was conducted for 3 consecutive days. The sham group and model group were administered the equivalent volume of physiological saline. The pharmacological effects of SMI on brain injury in MCAO/R rats were evaluated by neurological function scores, cerebral infarction area, hematoxylin-eosin (HE) staining, Nissl staining, terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining, and Western blot. The dominant link and key protein of SMI treating cerebral injury were explored using proteomic analysis. The related mechanisms of SMI were further validated using enzyme-linked immunosorbent assay (ELISA), Western blot, and chloride ion fluorescence probe with oxygen-glucose deprivation/reoxygenation(OGD/R)-treated PC12 cells and MCAO/R rats. ResultsCompared with the sham group, the model group showed significantly increased neurological function scores, cerebral infarction area, neuronal apoptosis rate, and expression levels of apoptosis related proteins (P<0.05, P<0.01)and significantly decreased density of Nissl bodies and neurons(P<0.01). Compared with the model group, the SMI groups exhibited significantly decreased neurological function scores, cerebral infarction area, neuronal apoptosis rate, and expression levels of apoptosis related proteins (P<0.05, P<0.01)and significantly increased density of Nissl bodies and neurons (P<0.05). The proteomic analysis results showed that oxidative stress and inflammatory response were important processes of SMI intervening in MCAO/R injury, and the chloride intracellular channel protein 1 (CLIC1) was one of key proteins in its action network. The levels of representative indicators of oxidative stress and inflammatory response in the MCAO/R rats of the SMI groups were significantly reduced, compared with those in the model group(P<0.05, P<0.01), and the expression levels of CLIC1 and downstream NOD-like receptor protein 3 (NLRP3) decreased (P<0.01). In addition, the experimental results based on the OGD/R PC12 cells showed that SMI significantly increased the cell survival rate(P<0.01) and significantly decreased the intracellular chloride ion concentration(P<0.05). ConclusionSMI has neuroprotective effects. Oxidative stress and inflammatory response are key processes of SMI intervening in MCAO/R injury. The potential mechanism is closely related to the regulation of CLIC1.