[Research progress of acupuncture mediated analgesia via regulating the function of endocannabinoid system].

Endocannabinoid system (ECS), which composed of its ligands and receptors, widely distributes in peripheral tissues and nerve system. Through complex regulating mechanisms, ECS exerts a variety of biological functions including analgesia. Its utility in analgesic regulation has attracted extensive attention, and the related achievements have also been transformed into clinical practice. With the deepened understanding of the essence of pain, as well as the advances in research techniques, quantity of research evidences showed that ECS could be regulated by acupuncture treatment and exerted analgesic effect in inflammatory pain, neuropathic pain and other related diseases, and the mechanism had also been revealed gradually. By reviewing literatures related to acupuncture analgesia and ECS, we summarized the effect and mechanism of acupuncture analgesia involved with regulation of ECS, pointed out cannabinoid (CB) 1 receptor and CB2 receptor exerted analgesic effect in central and peripheral neural system through mechanisms of inhibiting neural activation and anti-inflammation, respectively. Therefore, we hope to provide reference and inspiration for relevant research and clinical practice in the future.

APOBEC3B expression has prognostic significance in cervical cancer.

OBJECTIVE: Cervical cancer is one of the leading fatal diseases in women, and the role of Apolipoprotein B mRNA editing enzyme catalytic subunit 3B (APOBEC3B) in cervical cancer is uncertain. METHODS: Four Gene Expression Omnibus (GEO) mRNA microarray datasets were analyzed to identify differentially expressed genes (DEGs) between cervical cancer and normal cervical tissues. The results were validated using a The Cancer Genome Atlas (TCGA)-cervical cancer (CESC) dataset. Expression profiles and patients' clinical data were used to investigate the relationship between APOBEC3B expression and cervical cancer survival. APOBEC3B co-expressed genes were subjected to enrichment analyses, and correlations between APOBEC3B expression and immunologic infiltrates were investigated using Tumor Immune Estimation Resource (TIMER). We generated receiver operating characteristic curve (ROC) curves to evaluate the performance of APOBEC3B expression in predicting cervical cancer prognosis. RESULTS: Fourteen overlapping DEGs were obtained, and APOBEC3B was chosen as a candidate gene. TCGA data further confirmed that APOBEC3B was significantly increased in cervical cancer, relative to normal adjacent tissues, and this expression was associated with poor clinical outcome. Results from quantitative real time polymerase chain reaction (RT-qPCR) and immunohistochemical staining of cervical carcinoma tissues supported these findings. Enrichment analysis showed that APOBEC3B co-expressed genes were mainly enriched in cell cycle, DNA replication and chromosomal region. Moreover, APOBEC3B expression was significantly associated with T stage, M stage, primary therapy outcome and poor clinical prognosis in cervical cancer. Similarly, APOBEC3B was closely correlated with gene markers of diverse immune cells. APOBEC3B expression was an independent indicator of cervical cancer prognosis, according to univariate Cox and ROC analyses. CONCLUSION: High APOBEC3B expression is strongly related to a poor prognosis in cervical cancer patients.

Mitophagy in metabolic syndrome.

Metabolic syndrome (MS), a chronic and non-communicable pathological condition, is characterized by a constellation of clinical manifestations including insulin resistance, abdominal adiposity, elevated blood pressure, and perturbations in lipid metabolism. The prevalence of MS has increased dramatically in both developed and developing countries and has now become a truly global problem. Excessive energy intake and concomitant obesity are the main drivers of this syndrome. Mitophagy, in which cells degrade damaged mitochondria through a selective form of autophagy, assumes a crucial position in the regulation of mitochondrial integrity and maintenance. Abnormal mitochondrial quality could result in a spectrum of pathological conditions related to metabolic dysfunction, including metabolic syndrome, cardiovascular ailments, and neoplasms. Recently, there has been a proliferation of research pertaining to the process of mitophagy in the context of MS, and there are various regulatory pathways in MS, including pathways like the ubiquitin-dependent mechanism and receptor-mediated mechanisms, among others. Furthermore, studies have uncovered that the process of mitophagy serves a defensive function in the advancement of Metabolic Syndrome, and inhibition of mitophagy exacerbates the advancement of MS. As a result, the regulation of mitophagy holds great promise as a therapeutic approach in the management of Metabolic Syndrome. In this comprehensive analysis, the authors present a synthesis of the diverse regulatory pathways involved in mitophagy in the context of Metabolic Syndrome, as well as its modes of action in metabolic disorders implicated in the development of MS, Including obesity, insulin resistance (IR), and type 2 diabetes mellitus (T2DM), offering novel avenues for the prophylaxis and therapeutic management of MS.

[Effect of tranexamic acid combined flexion position of hip and knee on perioperative bleeding following unilateral total knee arthroplasty].

OBJECTIVE: To explore clinical efficacy and safety of application of tranexamic acid for two times combined with postoperative hip and knee on flexion position for reducing blood loss during total knee arthroplasty. METHODS: From January 2015 to January 2018, 90 patients with knee osteoarthritis underwent unilateral total knee arthroplasty, including 33 males and 57 females, aged from 61 to 85 years old with an average of(72.3±6.9) years old. The patients were randomly divided into three groups according to random number table, 30 patients in each group. In group A, there were 11 males and 9 females, aged from 61 to 84 years old with an average of (71.60±6.04) years old, body mass index was (26.04±1.95) kg/m², hemoglobin was(128.57±5.98) g/L, treated by 7.5 mg/kg tranexamic acid was injected intravenously before upper tourniquet, and 7.5 mg/kg tranexamic acid after closure of incision and before loosening tourniquet, meanwhile combined with flexion position of hip for 30° to 45° and flexion position of knee for 60° for 70°. In group B, there were 10 males and 20 females aged from 61 to 85 years old with an average of (72.04±7.47) years, body mass index was (25.92±1.70) kg/m², hemoglobin was (127.58±4.37) g/L, treated by 15 mg/kg tranexamic acid injected intravenously before loosening tourniquet. In group C, there were 12 males and 18 females aged from 62 to 85 years old with an average of (73.23±7.36) years, body mass index was (26.07±1.49) kg/m², hemoglobin was (128.31±5.61) g/L, treated with the same amount of normal saline before loosening tourniquet. Intraoperative bleeding volume, postoperative drainage volume, recessive blood loss, total blood loss volume, blood transfusion cases, activated partial thromboplastin time(APTT), prothrombin time(PT), prothrombin international standardized ratio (PT-INR) and indexes of D-dimer(D-D) were compared among three groups, as well as postoperative deep venous thrombosis and pulmonary embolism were observed among three groups. RESULTS: No incision infection occurred in all 90 patients, and all patients were followed up from 4 to 8 months with an average of 6 months without pulmonary embolism occurred. There was no statistical difference in itraoperative bleeding volume among three groups(F=0.299, P=0.742), while there were significant differences in postoperative drainage volume, recessive blood loss, and total blood loss among three groups. The number of blood transfusion were as following, 2 cases in group A, 8 cases in group B, and 16 cases in group C, there were statistically significant differences among three groups(χ² =16.01, P<0.001). There were no differences in APTT, PT, PT-INR and D-D after operation among three groups(P>0.05), and no difference in occurrence of lower limb vein thrombosis after operation. CONCLUSIONS: The method of using tranexamic acid before upper tourniquet, after closure of incision and before loosening tourniquet-combined with the flexion position of hip and knee could effectively reduce postoperative drainage volume, recessive bleeding, total blood loss and blood transfusion cases after total knee arthroplasty, while it does not increase risk of deep vein thrombosis and pulmonary embolism.

Short hairpin RNA-mediated knockdown of nuclear factor erythroid 2-like 3 exhibits tumor-suppressing effects in hepatocellular carcinoma cells.

BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors with high mortality-to-incidence ratios. Nuclear factor erythroid 2-like 3 (NFE2L3), also known as NRF3, is a member of the cap 'n' collar basic-region leucine zipper family of transcription factors. NFE2L3 is involved in the regulation of various biological processes, whereas its role in HCC has not been elucidated. AIM: To explore the expression and biological function of NFE2L3 in HCC. METHODS: We analyzed the expression of NFE2L3 in HCC tissues and its correlation with clinicopathological parameters based on The Cancer Genome Atlas (TCGA) data portal. Short hairpin RNA (shRNA) interference technology was utilized to knock down NFE2L3 in vitro. Cell apoptosis, clone formation, proliferation, migration, and invasion assays were used to identify the biological effects of NFE2L3 in BEL-7404 and SMMC-7721 cells. The expression of epithelial-mesenchymal transition (EMT) markers was examined by Western blot analysis. RESULTS: TCGA analysis showed that NFE2L3 expression was significantly positively correlated with tumor grade, T stage, and pathologic stage. The qPCR and Western blot results showed that both the mRNA and protein levels of NFE2L3 were significantly decreased after shRNA-mediated knockdown in BEL-7404 and SMMC-7721 cells. The shRNA-mediated knockdown of NFE2L3 could induce apoptosis and inhibit the clone formation and cell proliferation of SMMC-7721 and BEL-7404 cells. NFE2L3 knockdown also significantly suppressed the migration, invasion, and EMT of the two cell lines. CONCLUSION: Our study showed that shRNA-mediated knockdown of NFE2L3 exhibited tumor-suppressing effects in HCC cells.

Low expression of microRNA-340 confers adverse clinical outcome in patients with acute myeloid leukemia.

MicroRNA-340 (miR-340) was considered as a tumor suppressor by affecting cancer cell proliferation, apoptosis, invasion, and migration, and was downregulated in diverse cancers. Moreover, dysregulation of miR-340 was also found to be associated with drug resistance and predicted patients' survival in various cancers. Herein, we investigated miR-340 expression and its clinical significance in acute myeloid leukemia (AML). Real-time quantitative polymerase chain reaction was performed to detect miR-340 expression in bone marrow (BM) from 99 newly diagnosed AML patients except for acute promyelocytic leukemia (APL), 19 AML patients achieved complete remission (CR), and 29 healthy donors. BM miR-340 expression was significantly underexpressed in newly diagnosed AML patients as compared with controls (p = 0.031) and AML patients achieved CR (p = 0.025). No significant differences were observed between miR-340 expression and most of the clinicopathologic features (p > 0.05). However, low miR-340 expression was found to be associated with lower CR rate in both non-APL-AML and cytogenetically normal AML (CN-AML; p = 0.001 and 0.031, respectively), and acted as an independent risk factor for CR by logistic regression analysis (p = 0.001 and 0.021, respectively). More important, among both non-APL-AML and CN-AML, low expression of miR-340 was also associated with shorter overall survival (OS; p = 0.013 and 0.005, respectively), and was further validated by Cox regression (p = 0.031 and 0.039, respectively). Collectively, our study showed that BM miR-340 expression was downregulated in AML, and low expression of miR-340 correlated with adverse prognosis.

Increased apolipoprotein M induced by lack of scavenger receptor BI is not activated via HDL-mediated cholesterol uptake in hepatocytes.

BACKGROUND: Scavenger receptor BI (SR-BI) is a classic high-density lipoprotein (HDL) receptor, which mediates selective lipid uptake from HDL cholesterol esters (HDL-C). Apolipoprotein M (ApoM), as a component of HDL particles, could influence preß-HDL formation and cholesterol efflux. The aim of this study was to determine whether SR-BI deficiency influenced the expression of ApoM. METHODS: Blood samples and liver tissues were collected from SR-BI gene knockout mice, and serum lipid parameters, including total cholesterol (TC), triglyceride (TG), high and low-density lipoprotein cholesterol (HDL-C and LDL-C) and ApoM were measured. Hepatic ApoM and ApoAI mRNA levels were also determined. In addition, BLT-1, an inhibitor of SR-BI, was added to HepG2 cells cultured with cholesterol and HDL, under serum or serum-free conditions. The mRNA and protein expression levels of ApoM were detected by RT-PCR and western blot. RESULTS: We found that increased serum ApoM protein levels corresponded with high hepatic ApoM mRNA levels in both male and female SR-BI-/- mice. Besides, serum TC and HDL-C were also significantly increased. Treatment of HepG2 hepatoma cells with SR-BI specific inhibitor, BLT-1, could up-regulate ApoM expression in serum-containing medium but not in serum-free medium, even in the presence of HDL-C and cholesterol. CONCLUSIONS: Results suggested that SR-BI deficiency promoted ApoM expression, but the increased ApoM might be independent from HDL-mediated cholesterol uptake in hepatocytes.

Apolipoprotein M Protects Against Lipopolysaccharide-Induced Acute Lung Injury via Sphingosine-1-Phosphate Signaling.

It had been demonstrated that apolipoprotein M (apoM) is an important carrier of sphingosine-1-phosphate (S1P) in blood, and the S1P has critical roles in the pathogenesis of sepsis-induced acute lung injury (ALI). In the present study, we investigated whether apoM has beneficial effects in a mouse model after lipopolysaccharide (LPS)-induced ALI. Forty-eight mice were divided into two groups: male C57BL/6 wild-type (apoM+/+) group (n = 24) and apoM gene-deficient (apoM-/-) group (n = 24) and then randomly subdivided into four subgroups (n = 6 each) according to different intraperitoneal (i.p.) injection: control group, W146 group, LPS group, and LPS + W146 group. Serum levels of interleukin-1 beta (IL-1ß) and mRNA levels of IL-1ß, interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), lung histology, wet/dry weight ratio, and immunohistochemistry were measured at 3 h after the baseline and compared in each group. Our results clearly demonstrated that IL-1ß mRNA levels and other inflammatory biomarkers were significantly increased in the lungs of LPS-induced ALI apoM-/- mice compared to those of the apoM+/+ mice. Moreover, when apoM+/+ mice were treated with W146, a S1P receptor (S1PR1) antagonist, these inflammatory biomarkers could be significantly upregulated by LPS-induced ALI. Therefore, it suggests that apoM-S1P-S1PR1 signaling might underlie the pathogenesis of ALI and apoM could have physiological benefits to alleviate LPS-induced ALI.

Apolipoprotein M increases the expression of vitamin D receptor mRNA in colorectal cancer cells detected with duplex fluorescence reverse transcription-quantitative polymerase chain reaction.

Apolipoprotein M (ApoM) and the vitamin D receptor (VDR) are apolipoproteins predominantly presenting in high-density lipoprotein (HDL) and a karyophilic protein belonging to the steroid­thyroid receptor superfamily, respectively. Previous studies have demonstrated that ApoM and VDR are associated with cholesterol metabolism, immune and colorectal cancer regulation. In order to investigate whether ApoM affected the expression of VDR in colorectal cancer cells, a single­tube duplex fluorescence reverse transcription­quantitative polymerase chain reaction (RT­qPCR) system was developed to simultaneously detect the mRNA levels of VDR and GAPDH in HT­29 cells overexpressing ApoM. The results demonstrated that the amplification products were confirmed as the specific fragment of VDR/GAPDH using the DNA sequencing instrument. The sensitivity, linear range, correlation coefficient, amplification efficiency, intra­assay and inter­assay coefficients of variation were 40 copies/µl, 4.00x101­4.00x105 copies/µl, 0.999, 92.42%, 0.09­0.34% and 0.32­0.65% for VDR, and 40 copies/µl, 4.00x101­4.00x105 copies/µl, 0.999, 98.07%, 0.19­0.43% and 0.40­0.75% for GAPDH, respectively. The results indicated that the expression of VDR mRNA was significantly higher in HT­29 cells overexpressing ApoM, compared with the negative control group (P<0.05). In conclusion, the current study successfully developed the single­tube duplex RT­qPCR to simultaneously detect VDR and GAPDH expression in colorectal cancer cells. The methodology results demonstrated that the duplex RT­qPCR system with high sensitivity and specificity could ensure the objectivity and credibility of the detection. The present study confirmed that ApoM significantly increased the expression of VDR in HT­29 cells. In addition, it was hypothesized that ApoM may be involved in antineoplastic activity via the upregulation of VDR expression, which may provide novel directions for the investigation of ApoM in cancer.

17ß-estradiol regulates the expression of apolipoprotein M through estrogen receptor α-specific binding motif in its promoter.

BACKGROUND: We have previously demonstrated that estrogen could significantly enhance expression of apolipoprotein M (apoM), whereas the molecular basis of its mechanism is not fully elucidated yet. To further investigate the mechanism behind the estrogen induced up-regulation of apoM expression. RESULTS: Our results demonstrated either free 17ß-estradiol (E2) or membrane-impermeable bovine serum albumin-conjugated E2 (E2-BSA) could modulate human apoM gene expression via the estrogen receptor alpha (ER-α) pathway in the HepG2 cells. Moreover, experiments with the luciferase activity analysis of truncated apoM promoters could demonstrate that a regulatory region (from-1580 to -1575 bp (-GGTCA-)) upstream of the transcriptional start site of apoM gene was essential for the basal transcriptional activity that regulated by the ER-α. With the applications of an electrophoresis mobility shift assay and a chromatin immunoprecipitation assay, we could successfully identify a specific ER-α binding element in the apoM promoter region. CONCULSION: In summary, the present study indicates that 17ß-estradiol induced up-regulation of apoM in HepG2 cells is through an ER-α-dependent pathway involving ER-α binding element in the promoter of the apoM gene.

miR-590 promotes cell proliferation and invasion in T-cell acute lymphoblastic leukaemia by inhibiting RB1.

MicroRNAs play important roles in the pathogenesis of cancers by inhibiting gene expression at posttranscriptional level. Here, we identified that miR-590 and its predicted target gene RB1 are differentially expressed in T-cell acute lymphoblastic leukaemia (T-ALL). The correlation between miR-590 and RB1 was further confirmed in 395 T-ALL patients. In T-ALL cell lines, miR-590 promoted the cell proliferation by increasing G1/S transition. Moreover, migration and invasion assay showed that miR-590 promotes the migration and invasion of T-ALL cells by increasing E-cadherin and inhibiting MMP-9. Luciferase assays confirmed that miR-590 directly binds to the 3'untranslated region of RB1, and western blotting showed that miR-590 suppresses the expression of RB1 at the protein levels. This study indicated that miR-590 inhibits RB1 and promotes proliferation and invasion of T-ALL cells. Thus, miR-590 may represent a potential therapeutic target for T-ALL intervention.

Clinical Trial Research on Mongolian Medical Warm Acupuncture in Treating Insomnia.

Objective. Insomnia is one of the most common sleep disorders. Hypnotics have poor long-term efficacy. Mongolian medical warm acupuncture has significant efficacy in treating insomnia. The paper evaluates the role of Mongolian medical warm acupuncture in treating insomnia by investigating the Mongolian medicine syndromes and conditions, Pittsburgh sleep quality index, and polysomnography indexes. Method. The patients were diagnosed in accordance with International Classification of Sleep Disorders (ICSD-2). The insomnia patients were divided into the acupuncture group (40 cases) and the estazolam group (40 cases). The patients underwent intervention of Mongolian medical warm acupuncture and estazolam. The indicators of the Mongolian medicine syndromes and conditions, Pittsburgh sleep quality index (PSQI), and polysomnography indexes (PSG) have been detected. Result. Based on the comparison of the Mongolian medicine syndrome scores between the warm acupuncture group and the drug treatment group, the result indicated P < 0.01. The clinical efficacy result showed that the effective rate (85%) in the warm acupuncture group was higher than that (70%) in the drug group. The total scores of PSQI of both groups were approximated. The sleep quality indexes of both groups decreased significantly (P < 0.05). The sleep quality index in the Mongolian medical warm acupuncture group decreased significantly (P < 0.01) and was better than that in the estazolam group. The sleep efficiency and daytime functions of the patients in the Mongolian medical warm acupuncture group improved significantly (P < 0.01). The sleep time was significantly extended (P < 0.01) in the Mongolian medical warm acupuncture group following PSG intervention. The sleep time during NREM in the Mongolian warm acupuncture group increased significantly (P < 0.01). The sleep time exhibited a decreasing trend during REM and it decreased significantly in the Mongolian warm acupuncture group (P < 0.01). The percentage of sleep time in the total sleep time during NREM3+4 in the Mongolian medical warm acupuncture group increased significantly. Conclusion. Mongolian medical warm acupuncture is efficient and safe in treating insomnia. It is able to better improve the patients' sleep time and daytime functions. It is better than that in the estazolam group following drug withdrawal in terms of improving the sleep time. It is more effective in helping the insomnia patients than hypnotics.

The Down-Regulation of MicroRNA-497 Contributes to Cell Growth and Cisplatin Resistance Through PI3K/Akt Pathway in Osteosarcoma.

BACKGROUND: Down-expression of microRNA-497 (miR-497) was often found in malignancies. The purposes of this study were to determine the expression of miR-497 in human osteosarcoma and to establish the association between miR-497 expression with cell survival and the sensitivity to cisplatin in human osteosarcoma cells. METHODS: The effects of ectopic miR-497 expression on the cell survival and cisplatin sensitivity in osteosarcoma cells were measured by the Cell Counting Kit-8 (CCK-8) assay. Quantitative real-time PCR (qRT-PCR) was utilized to determine the expression of miR-497. The effects of ectopic miR-497 expression on the expression of VEGFA, Akt and p-Akt were determined by western blot. RESULTS: Real-time quantitative PCR analysis revealed that miR-497 was significantly down-regulated in osteosarcoma tissues and in the osteosarcoma cell line SAOS-2 compared with adjacent nontumorous osteosarcoma tissues and normal human osteoblasts. Up-regulation of miR-497 inhibited cell survival and enhanced the sensitivity to cisplatin in osteosarcoma cells. In addition, knockdown of miR-497 induced osteosarcoma cells growth and cisplatin resistance. Luciferase reporter assay and western blot confirmed that VEGFA was a direct target of miR-497. PI3K inhibitor LY294002 abrogated miR-497 inhibitors induced cisplatin resistance. CONCLUSION: Taken together, our results suggest that miR-497 modulates the sensitivity to cisplatin at least in part through PI3K/Akt pathway in osteosarcoma cells.

miR-664 negatively regulates PLP2 and promotes cell proliferation and invasion in T-cell acute lymphoblastic leukaemia.

MicroRNAs (miRNAs) play important roles in the pathogenesis of many types of cancers by negatively regulating gene expression at posttranscriptional level. However, the role of microRNAs in leukaemia, particularly T-cell acute lymphoblastic leukaemia (T-ALL), has remained elusive. Here, we identified miR-664 and its predicted target gene PLP2 were differentially expressed in T-ALL using bioinformatics methods. In T-ALL cell lines, CCK-8 proliferation assay indicated that the cell proliferation was promoted by miR-664, while miR-664 inhibitor could significantly inhibited the proliferation. Moreover, migration and invasion assay showed that overexpression of miR-664 could significantly promoted the migration and invasion of T-ALL cells, whereas miR-664 inhibitor could reduce cell migration and invasion. luciferase assays confirmed that miR-664 directly bound to the 3'untranslated region of PLP2, and western blotting showed that miR-664 suppressed the expression of PLP2 at the protein levels. This study indicated that miR-664 negatively regulates PLP2 and promotes proliferation and invasion of T-ALL cell lines. Thus, miR-664 may represent a potential therapeutic target for T-ALL intervention.

[Significance of interplay between Rap1 and cadherin to the development of myelodysplastic syndrome].

OBJECTIVE: To explore the hematopoietic pathophysiology of myelodysplastic syndrome (MDS) at stem/progenitor cell level by analyzing the gene expression profiles associated with hematopoiesis. METHODS: The differentially expressed genes which were involved in the hematopoiesis were screened by microarray using CD34(+) cells from MDS patients firstly. RQ-PCR was then applied to validate the screened genes using CD34(+) cells from MDS-RA patients who had normal karyotype. The linkages with hematopoiesis among these validated genes were analyzed. RESULTS: Among the differentially expressed genes in CD34(+) cells of MDS-RA patients, Rap1GAP was up-regulated significantly (P < 0.01). Cadherins, which can interplay with Rap1, including N-cadherin and E-cadherin, were down-regulated significantly (P < 0.01). ß-catenin, a downstream effector of cadherins, was highly expressed in MDS-RA patients (P < 0.01). c-myc binding protein was down-regulated (P < 0.01), and c-myc promoter binding protein was up-regulated (P < 0.01). Rac1, Rac2 and Cdc42, which belong to RhoGTPases family and are associated with the cell morphology and hematopoiesis, were all expressed highly in MDS-RA patients (P < 0.01). CONCLUSION: The abnormal expression of cadherin, ß-catenin and c-myc associated genes were closely related to the dysplastic hematopoiesis of MDS. The down regulation of cadherin was associated with the positive feedback mechanism between Rap1 and cadherin. The aberrant expression of Rac1, Rac2 and Cdc42 may contribute to the morphological dysplasia of MDS.

[Clinical study of heparin-induced thrombocytopenia].

OBJECTIVE: To observe the incidence of heparin-induced thrombocytopenia (HIT) in patients received unfractionated heparin (UFH) treatment, and explore the feasibility of monitoring HIT by platelet counts, as well as the significance of HIT-antibody test in HIT diagnosis. METHODS: 145 patients received UFH treatment in Vascular Surgery Department were studied. Before and after the UFH treatment, platelet counts, HIT-antibody ELISA test and heparin-induced platelet aggregation (HIPA) were tested. RESULTS: Among the 145 patients, thrombocytopenia occurred in 40 (27.6%) cases, HIT-antibody ELISA test positive in 59 (40.7%) cases, HIPA test positive in 26 (17.9%) cases. The HIT was diagnosed in 24 (16.5%) cases, and heparin-induced thrombocytopenia and thrombosis (HITTS) occurred in 5 (3.4% in all cases, and 20.8% in HIT patients). In HIT patients, 15 patients (62.5%) were thrombocytopenia, HIT-antibody positive and HIPA test positive. Platelet counts in all of the 24 patients recovered to normal or level before UFH treatment in 3-6 days after heparin withdrawal therapy. CONCLUSION: HIT can be early diagnosed by monitoring platelet counts, HIT-antibody ELISA test and HIPA test. Withdrawal of heparin therapy in time and use of alternative anticoagulant, HITTS rate might be expected to decline further.