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Objective:To investigate the serum level of fatty acid binding protein 1 (FABP1) and its relationship with Helicobacter pylori (Hp) infection in patients with gastric cancer. Methods:Forty gastric cancer patients (gastric cancer group) who were hospitalized in Affiliated Hospital of Qinghai University from August 2021 to August 2022 were selected as the research subjects, and 40 physical examination subjects during the same period were selected as the normal control group and 40 chronic atrophic gastritis patients were selected as the CAG group. The Hp infection were detected by 13C breath test, and the levels of serum FABP1 were detected by enzyme-linked immunosorbent assay. The Hp infection status, serum FABP1 levels, and the relationship between the two in the three groups of study subjects were analyzed. And the relationships between the level of serum FABP1 and the clinicopathological features of gastric cancer patients were analyzed. The diagnostic value of serum FABP1, CA19-9, CA72-4 and combined test of 3 indexes were evaluated by receiver operating characteristic (ROC) curve. Results:The Hp infection rates in the control group, CAG group, and gastric cancer group were 32.50% (13/40), 55.00% (22/40), and 60.00% (24/40), respectively, with a statistically significant difference ( χ2=6.87, P=0.032). Among them, the Hp infection rate in the control group was compared with that in the gastric cancer group, with a statistically significant difference ( P<0.05), and there were no statistically significant differences between the CAG group and the control group, the gastric cancer group (both P>0.05). The levels of serum FABP1 in the control group, CAG group, and gastric cancer group were [63.47 (37.53, 71.59) ] ng/ml, [65.26 (51.15, 79.67) ] ng/ml, and [72.84 (53.44, 82.25) ] ng/ml, respectively, with a statistically significant difference ( H=6.62, P=0.037). Among them, there was a statistically significant difference between the control group and the gastric cancer group ( H=19.93, P=0.031), while there were no statistically significant differences between the CAG group and the control group, the gastric cancer group ( H=1.50, P=0.133; H=1.09, P=0.277). Among all study subjects, the levels of serum FABP1 in the Hp positive group ( n=59) and Hp negative group ( n=61) were [77.05 (68.90, 83.54) ] ng/ml and [47.80 (37.76, 63.32) ] ng/ml, respectively, with a statistically significant difference ( Z=7.45, P<0.001). In the control group, the levels of FABP1 in the serum of Hp positive and Hp negative persons were [77.34 (68.84, 86.31) ] ng/ml and [39.79 (36.83, 63.75) ] ng/ml, respectively, with a statistically significant difference ( Z=4.46, P<0.001). In the CAG group, the levels of FABP1 in the serum of Hp positive and Hp negative patients were [76.51 (65.30, 80.97) ] ng/ml and [49.34 (39.92, 59.41) ] ng/ml, respectively, with a statistically significant difference ( Z=4.32, P<0.001). In the gastric cancer group, the levels of FABP1 in the serum of Hp positive and Hp negative patients were [77.15 (72.62, 84.13) ] ng/ml and [50.57 (44.54, 68.97) ] ng/ml, respectively, with a statistically significant difference ( Z=4.32, P<0.001). There were significant correlations between the serum level of FABP1 and smoking ( t=2.54, P=0.015), tumor diameter ( t=2.23, P=0.035), and lymph node metastasis ( t=3.22, P=0.003) in gastric cancer patients. And there were no significant correlations between FABP1 and gender ( t=0.98, P=0.333), age ( t=1.60, P=0.117), alcohol consumption ( Z=0.10, P=0.925), tumor site ( F=1.06, P=0.356), degree of differentiation ( t=0.61, P=0.545), the depth of infiltration ( t=1.41, P=0.166), distant metastasis ( Z=1.96, P=0.050) and TNM staging ( Z=0.66, P=0.508). ROC curve analysis showed that the area under the curve (AUC) of serum FABP1 for gastric cancer diagnosis was 0.62, 95% CI: 0.51-0.72, the sensitivity and specificity were 57.50% and 68.70%, respectively; the AUC of CA19-9 for gastric cancer diagnosis was 0.89, 95% CI: 0.83-0.95, the sensitivity and specificity were 77.50%, 86.30%, respectively; the AUC of CA72-4 for gastric cancer diagnosis was 0.88, 95% CI: 0.81-0.94, the sensitivity and specificity were 70.00%, 93.70%, respectively; the AUC of combined test of 3 indexes for gastric cancer diagnosis was 0.91, 95% CI: 0.82-0.97, the sensitivity and specificity were 67.50% and 95.00%, respectively. Conclusion:The Hp infection rate of gastric cancer patients is higher than that of the health examiners, the serum FABP1 level of gastric cancer patients is higher than that of the healthy health examiners, the serum FABP1 level of Hp positive persons is higher than that of Hp negative persons, and Hp infection and FABP1 level may have a common carcinogenic mechanism in the occurrence and development of gastric cancer.
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As an effective treatment for cancer, chemotherapy not only removes tumor cells, but also produces obvious killing effects on proliferating cells, especially hematopoietic cells, resulting in bone marrow suppression after chemotherapy, and affecting the effects of chemotherapy drug treatment and treatment cycle. Therefore, starting from the aspects of hematopoietic microenvironment damage and hematopoietic stem cell aging, to explore the mechanism of myelosuppression after chemotherapy, which provides new ideas and theoretical support for the intervention and management of bone marrow suppression after cancer chemotherapy.
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Immune checkpoint inhibitor (ICI) has become one of the important therapeutic strategies for the patients with advanced non-small cell lung cancer (NSCLC). The latest clinical studies have shown that immunotherapy can bring more survival benefits to patients with early lung cancer and operable patients with locally advanced lung cancer. However, the strategies of neoadjuvant immunotherapy, the timing of operation, the evaluation system of curative effect, predictive markers and other problems still need to be explored in the clinical practice of large samples. This paper reviews the progress of neoadjuvant immunotherapy in NSCLC.
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Objective:To study the expression of miRNA-7 in B lymphocytes of primary Sj?gren's syndrome (pSS) and its relationship with phosphatase andtensin homolog deleted (PETN) and disease activity.Methods:Twenty newly diagnosed outpatient and inpatient pSS patients were used as case group collected from January 2017 to December 2019 of Qinghai Provincial People's Hospital. Twentyhealthy persons were used as the control group. Disease-related indicators of the case group were collected. Quantitative polymerase chain reaction (RT-qPCR)was used to detect miRNA-7 and PETN mRNA expression in B lymphocytes of the two groups and the consistency between miRNA-7 expression in the plasma and B lymphocytes of the case group was analyzed. Western Blotting method was used to detect the PETN protein in B lymphocytes of the two groups. Correlation analysis was used to analyze the relationship between miRNA-7 expression in B lymphocytes and disease activity in the case group. Linear regression analysis was performed between miRNA-7 and PETN mRNA.Results:The expression of miRNA-7 (0.53±0.17) in the B cells increased and the expression of PTEN mRNA (0.88± 0.24) and protein (0.51±0.12) in the case group were reduced compared with that of miRNA-7(0.39±0.11), PTEN mRNA(2.32±0.30) and protein(1.03±0.21) of the control group. The above differences were statistically significant ( t=2.990, P<0.05; t=16.98, P<0.05; t=8.41, P<0.05). Linear regression showedthat PTEN miRNAwas negatively correlated with miRNA-7 ( b=-0.78, P<0.01), the expression of miRNA-7 in the case group was positively related with EULAR Sj?gren′s syndrome Disease Activity Index (ESSDAI), IgG, IgA, anti-SSB and was negatively correlated with C4 and WBC. Conclusion:There is a certain relationship between miRNA-7 and disease activity. MiRNA-7 may participate in the pathogenesis of pSS byregulating PETN in B cells of pSS. MiRNA-7 has certain clinical value for disease activity evaluation.
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Brain is the most common site of lung cancer metastasis, and the incidenceis are higher if patients have driver gene mutation. Patients with brain metastasis have a poor prognosis; further, different treatment methods affect the disease status and prognosis. In recent years, with the development of precision medicine, gradual progress has been made in treatments for lung cancer patients with brain metastasis, especially for those with driver gene mutations. This review first highlights the challenges of brain metastasis treatments, and then summarizes the research progress regarding targeted therapies for patients with driver gene mutation-positive lung cancer and brain metastasis. This review could help guide clinical decision making for individualized treatment in daily clinical practice.
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Objective To investigate the expression of miR-372 in the plasma of patients with acute my-eloid leukemia(AML)and the possible mechanism to participate in the development of AML. Methods Real-time quantitative PCR was used to detect the level of miR-372 in plasma. Bioinformatics software predicted the pos-sible target genes of miR-372 and dual luciferase reporter assay was performed to validate the prediction. In HL-60 cells,miR-372 was knocked down,and the effects on cell migration and cloning were detected by scratch test and clone formation. Results The level of miR-372 was significantly up-regulated in the plasma of AML patients. ROC analysis showed that miR-372 could distinguish between AML patients and healthy controls. Dual luciferase report-er assay showed that miR-372 could inhibit the activity of PTEN-3'UTR. Inhibition of miR-372 in HL-60 cells can significantly reduce the cell migration rate and clone formation ability. Conclusion In summary,for the first time,we showed novel data that the level of miR-372 was increased in the plasma of AML patients. By targeting the tumor suppressor gene PTEN,miR-372 may become a potential noninvasive biomarker for the screening and di-agnosis of AML.
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Objective To evaluate the role of the angiotensin Ⅱ type 2 receptor (AT2R) in repeated propofol anesthesia-induced neuroapoptosis in the basal ganglia of newborn rats.Methods Fiftyfour pathogen-free Sprague-Dawley rats,aged 7 days,weighing 10-15 g,were divided into 3 groups (n=18 each) using a random number table:control group (group C),repeated propofol anesthesia group (group P) and AT2R agonist CGP42112A group (group G).In group C,0.9％ sodium chloride injection 3 ml/kg was intraperitoneally injected,and half of the initial dose 1.5 ml/kg was given every 20 min for 5 times in total,lasting for 3 consecutive days.In group P,propofol 30 mg/kg was intraperitoneally injected,and half of the initial dose 15 mg/kg was given every 20 min for 5 times in total,lasting for 3 consecutive days.In group G,CGP42112A 1 mg/kg was intraperitoneally injected,propofol 30 mg/kg was intraperitoneally injected 5 min later,and half of the initial dose of propofol 15 mg/kg was given every 20 min for 5 times in total,lasting for 3 consecutive days.Six rats were sacrificed at 2 h after emergence from anesthesia,and brains were removed for detection of neuroapoptosis in the basal ganglia by TUNEL assay.The apoptosis index was calculated.Another 6 rats were sacrificed,and the basal ganglia were isolated from brains to detect the expression of activated caspase-3,AT2R and peroxisome proliferator-activated receptor gamma (PPARγ) (by Western blot) and the expression of AT2R and PPARγ mRNA (by real-time polymerase chain reaction).The other 6 rats were fed until 28 days old,and the cognitive function was then assessed using Morris water maze test.Results Compared with group C,the escape latency was significantly prolonged,the time of staying at the target quadrant was shortened,the frequency of crossing the platform was decreased,the apoptosis index of the basal ganglia was increased,the expression of activated caspase-3 was up-regulated,and the expression of AT2R and PPARγprotein and mRNA was down-regulated in group P (P＜0.05),and no significant change was found in the parameters mentioned above in group G (P＞0.05).Compared with group P,the escape latency was significantly shortened,the time of staying at the target quadrant was prolonged,the frequency of crossing the platform was increased,the apoptosis index of the basal ganglia was decreased,the expression of activated caspase-3 was down-regulated,and the expression of AT2R and PPARγ protein and mRNA was up-regulated in group G (P＜0.05).Conclusion Inhibited activation of AT2R is involved in repeated propofol anesthesia-induced neuroapoptosis in the basal ganglia of newborn rats.
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Objective To evaluate the relationship between propofol anesthesia and postoperative delirium and inflammatory responses of aged rats.Methods Twenty-four adult male Sprague-Dawley rats,aged 18 months,weighing 550-650 g,were divided into 3 groups (n=8 each) using a random number table method:control group (group C),propofol anesthesia for 2 h group (group P2) and propofol anesthesia for 4 h group (group P4).In P2 and P4 groups,anesthesia was maintained with propofol at a rate of 24 mg· kg-1 · h-1 for 2 and 4 h,respectively,after anesthesia was induced with propofol.Morris water maze test was performed at 1 day before and after anesthesia.Blood and cerebrospinal fluid samples were collected after the end of Morris water maze test for determination of interleukin-1beta (IL-1β),IL-4,IL-6 and tumor necrosis factor-alpha (TNF-α) concentrations in plasma and cerebrospinal fluid by enzyme-linked immunosorbent assay.The hippocampus and cortex were removed for determination of Iba-1 positive cells.Results Compared with group C and the baseline value before anesthesia,no significant change was found in the escape latency or percentage of time of staying at the original platform quadrant in P2 and P4 groups (P＞0.05),the concentrations of IL-6 in cerebrospinal fluid and TNF-α in plasma were significantly decreased in group P2,the concentrations of IL-1β in cerebrospinal fluid and IL-4,IL-6 and TNF-α in plasma were significantly increased,and the concentrations of IL-1β in plasma and IL-4 in cerebrospinal fluid were decreased in group P4,and the number of hippocampal Iba-1 positive cells were significantly decreased in P2 and P4 groups (P＜0.05 or 0.01).Conclusion Propofol anesthesia dose not induce postoperative delirium and central inflammatory responses within 4 h,and propofol can induce peripheral inflammatory responses when anesthesia time is longer than 2 h.
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Objective:To investigate the effect of sufentanil in preventing the adverse effects of hamabate in the patients undergoing cesarean section.Methods:Forty patients who would have been injected with hamabate were selected,they were undergoing elective cesarean section with continuous epidural anesthesia and randomly divided into sufentanil group and 0.9％ sodium chloride injection group.When the fetus was removed and hamabate was injected,simultaneously patients in sufentanil group were injected sufentanil 0.1 μg/ kg,and patients in 0.9％ sodium chloride group were injected equal dose of normal saline.MAP,HR,SpO2 and RR were monitored in the two groups.Adverse reactions after hamabate injecting into the body of the uteru,such as nausea,vomiting,chest pain,dizziness and facial flushing were recorded,and Ramsay sedation score was recorded before anesthesia,at 30 min after hamabate was injected and at the ending of the operation.Results:After 30 min using hamabate,MAP,H R and RR of sufentanil group were more stable than 0.9％ sodium chloride group(P ＜ 0.05),Ramsay sedation score of sufentanil group was higher than 0.9％ sodium chloride group(P＜0.05).Adverse reactions such as nausea,chest pain,dizziness and facial flushing were lower in sufentanil group than those in 0.9％ sodium chloride group(P ＜0.05).Conclusions.Small doses of sufentanil can reduce the adverse effects of hamabate in cesarean section,and hemodynamic can be more stable,also it is a certain better sedation,and can be usesd safely.
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Objective:To investigate the expression of SHIP1 in the patients with acute myeloid leukemia and its effect on the apoptosis of human leukemia cells.Methods:The expression of SHIP1 in the bone marrow of patients with acute myeloid leukemia was detected by Westem blot.U937 cells was transfected with SHIP1 expression vector (pEGFP-SHIP1 group) and empty vector control (pEGFP group) respectively,U937 cells without transfection were used as the control group.Flow cytometry was used to detect the apoptosis of the cells,the expression of SHIP1,Bcl-2,Bax,Akt,p-Akt were detected by western blot.Results:The expression of SHIP1 in the bone marrow of patients with acute myeloid leukemia was significantly lower than that of the normal human bone marrow SHIP 1 (P＜0.01).The SHIP1 and Bax expressions as well as the apoptotic rate ofpEGFP-SHIP1 group were significantly higher than those of the control group(P＜0.01),while the Bcl-2 and p-Akt expressions were significantly lower than those in the control group(P＜0.01).Conclusions:SH-P1 expression was down regulated in the bone marrow of patients with acute myeloid leukemia.SHIP1 could promote the apoptosis of human leukemia cells via Akt signaling pathway.
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Objective To evaluate the role of the angiotensin Ⅱ type 2 receptor (AT2R) in repeated propofol anesthesia-induced neuroapoptosis in the hippocampus of newborn rats.Methods Fiftyfour pathogen-free Sprague-Dawley rats,aged 7 days,weighing 10-15 g,were divided into 3 groups (n=18 each) using a random number table:control group (group C),repeated propofol anesthesia group (group P) and AT2R agouist CGP42112A group (group G).In group C,0.9％ sodium chloride injection 3 ml/kg was intraperitoneally injected,and half of the initial dose 1.5 ml/kg was given every 20 min for 5 times in total,lasting for 3 consecutive days.In group P,propofol 30 mg/kg was intraperitoneally injected,and half of the initial dose 15 mg/kg was given every 20 min for 5 times in total,lasting for 3 consecutive days.In group G,a single bolus of CGP42112A 1 mg/kg was intraperitoneally injected,propofol 30 mg/kg was intraperitoneally injected 5 min later,and half of the initial dose of propofol 15 mg/kg was given every 20 min for 5 times in total,lasting for 3 consecutive days.At 2 h after emergence from anesthesia,6 rats were sacrificed and brains were removed for detection of neuroapoptosis in the hippocampus by TUNEL assay.The apoptosis index was calculated.Another 6 rats were sacrificed,brains were removed and hippocampi were isolated for determination of the expression of activated caspase-3,AT2R and peroxisome proliferator-activated receptor gamma (PPARγ) in hippocampal tissues by Western blot.The other 6 rats were fed until 28 days old,and the cognitive function was then assessed using Morris water maze test.Results Compared with group C,the escape latency was significantly prolonged,the time of staying at the target quadrant was shortened,the frequency of crossing the platform was decreased,the apoptosis index was increased,the expression of activated caspase-3 was up-regulated,and the expression of AT2R and PPARγ was down-regulated in group P (P＜0.05),and no significant change was found in the parameters mentioned above in group G (P＞0.05).Compared with group P,the escape latency was significantly shortened.the time of staying at the target quadrant was prolonged,the frequency of crossing the platform was increased,the apoptosis index was decreased,the expression of activated caspase-3 was down-regulated,and the expression of AT2R and PPARγ was up-regulated in group G (P＜0.05).Conclusion Inhibited activity of AT2R is involved in repeated propofol anesthesia-induced neuroapoptosis in the hippocampus of newborn rats.
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Objective To evaluate the relationship between the mechanism of spinal monocyte chemoattractant protein-1 (MCP-1)-mediated maintenance of chronic pathological pain and synaptic transmission in spinal dorsal horns of rats.Methods Female Sprague-Dawley rats,aged 2-3 weeks after birth,weighing 150-210 g,were studied.The experiment was performed in 2 parts.Experiment Ⅰ Eighteen Sprague-Dawley rats were randomly divided into 2 groups (n =9 each) on 7 days after intrathecal catheters were inserted:phosphate buffer solution (PBS) group and MCP-1 group.PBS 10 μl was intrathecally injected in group PBS,and PBS 10 μ1 containing 100 ng MCP-1 was intrathecally injected in group MCP-1.The mechanical pain threshold was measured at 30 and 60 min before intrathecal injection,and 30,60,90,120,150 and 180 min and 1,2 and 3 days after intrathecal injection.Experiment Ⅱ The transverse spinal cord slices were prepared,and substantia gelatinosa neurons were selected for whole-cell patch-clamp recording.Electrophysiological recording was performed at 1 h of incubation with artificial cerebrospinal fluid (ACSF) and immediately after adding MCP-1:for excitatory synaptic transmission recording,MCP-1 (final concentration 100 nmol/L),N-methyl-D-aspartate (NMDA,final concentration 100 μmol/L) and α-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA,final concentration 20 μmol/L) were added to ACSF,and spontaneous excitatory postsynaptic currents (sEPSCs),AMPA receptors-mediated currents and NMDA receptors-mediated currents were recorded;for inhibitory synaptic transmission recording,MCP-1 (final concentration 100 nmol/L) and γ-aminobutyric acid (GABA,final concentration 1 mmol/L) were added to ACSF,and spontaneous inhibitory postsynaptic currents (sIPSCs) and GABA receptors-mediated currents were recorded.Results Compared with group PBS,the mechanical pain threshold was significantly decreased at 30 min-2 days after intrathecal injection in group MCP-1 (P＜0.01).Compared with those at 1 h of incubation with ACSF,the frequency and amplitude of sEPSCs were significantly increased,the amplitude of NMDA receptors-and AMPA receptors-mediated currents were increased,the frequency and amplitude of sIPSCs were decreased,and the amplitude of GABA receptors-mediated currents was decreased immediately after adding MCP-1 (P＜0.05).Conclusion MCP-1 enhances excitatory synaptic transmission through enhancing the function of NMDA and AMPA receptors in the posterior substantia gelatinosa neurons of the spinal cord;MCP-1 weakens inhibitory synaptic transmission through inhibiting GABA receptor function,which may be involved in MCP-l-mediated maintenance of chronic pathological pain in rats.
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Objective To explore the clinical significance of a series of cytokines and peripheral blood immunocyte subsets before and after immunosuppressive therapy in patients with immune thrombocytopenia (ITP).Methods The percentages of immunocyte subsets in the peripheral blood of 20 patients with ITP and 20 healthy controls were detected by flow cytometry,including CD3+,CD4+,CD8+,CD4+/CD8+,CD1~.ELISA was applied to detect the level of serum TNFα,IL-2,IL-6,IL-4,IL-10,IL-11,IL-17,IL-27,transforming growth factor β (TGFβ),thrombopoietin (TPO) of 20 patients with ITP and 20 healthy controls.Results The percentage of CD3+ T lymphocyte,CD4+ T lymphocyte and the ratio of CD4+ / CD8+ T lymphocyte in patients with ITP were lower than those in healthy controls [(62.66 ± 6.58) ％ vs (69.93 ± 4.81) ％,(29.46 ± 5.02) ％ vs (39.08 ± 3.50) ％,0.97 ± 0.35 vs 1.56 ± 0.26,all P ＜ 0.05].After immunosuppressive therapy,the percentage of CD3+ T lymphocyte,CD4+ T lymphocyte and the ratio of CD4+/CD8+ T lymphocyte [(71.49 ±5.16)％,(39.25 ±3.21)％ and 1.56 ±0.28] recovered to the same levels in healthy controls.The percentage of CD8+ T lymphocyte and CD19+ B lymphocyte in patients with ITP were higher than those in the healthy controls [(30.28 ±4.63)％ vs (25.90±3.06)％,(18.92 ± 4.27)％ vs (13.17 ± 3.64)％,all P ＜ 0.05].After treatment of immunosuppressive therapy,the percentage of CD8+ T lymphocyte and CD19+ B lymphocyte [(25.16 ± 3.45) ％ and (11.98 ± 3.68) ％] recovered to the similar levels in healthy controls.The serum levels of IL-4,IL-6,IL-11,IL-17 and TPO in patients with ITP were significantly higher than those in healthy controls.While TGFβ level was significantly decreased.There was no significant difference of IL-27 between ITP patients and healthy controls.After the treatment of immunosuppressive therapy,IL-4,IL-6,IL-11,IL-17,TPO and TGFβ were down-regulated while IL-27 was up-regulated.There was no significant difference of IFNγ,TNFα,IL-2 and IL-10 among ITP patients before or after immunosuppressive therapy and healthy controls.Conclusions The present study suggests that the aberrant immunocyte subsets and cytokines are involved in the pathogenesis of ITP.Hyper-function of Th2 and Th17,dysfunction of Treg cells,up-regulation of IL-27,IL-11,TPO and other factors may contribute to the pathogenesis of ITP.
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With the research progress of pathogenesis of JAK gene in myeloproliferative neoplasms (MPN), more tyrosine kinase inhibitors were developed. MPN quantify scoring system is used to determine the efficacy of tyrosine kinase inhibitors for MPN. The choice of tyrosine kinase inhibitors, tyrosine kinase for the relief of MPN symptom burden, etc, become the topics of the 57th American Society of Hematology (ASH) annual meeting.
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Objective To analyze the changes and clinical significance of C-reactive protein (CRP)、hemoglobin (Hb) and erythrocyte sedimentation rate (ESR) in different disease stage of multiple myeloma according the international staging system. Method Thirty untreated MM patients with complete clinical records were included in the stndy. The multiple myeloma patients were classified into three groups according to international staging system (ISS).Thirty megaloblastic anemia patients of similar age 、sex、hemoglobin level as the observation group.Resulets The levels of CRP (24.17±9.87 mg/L)、Hb (71.72±13.27 g/L) and ESR (105.94±27.73 mm/h) of stage Ⅲ patients were statistically different with stage Ⅰ ( CRP 8.54±1.97 mg/L; Hb 91.00±9.92g/L; ESR 73.57±20.53mm/h)、Ⅱ patients ( CRP 14.89±5.51 mg/L; Hb 91.29±8.32g/L; ESR 67.00± 15.56 mm/h) separately (P＜0.05).The levels of CRP (19.40±10.17 mg/L) and ESR (91.90±29.70 mm/h) in the MM patients were significantly higher than that in the observation group Ⅰ ( CRP 7.52±1.57mg/L; ESR 20.20±8.04mm/h) (P＜0.05 respectively).CRP and ESR level in MM patients positively correlated with myeloma cell proportion and β2-microglobulin level (P＜0.05), while Hb level negatively correlated with myeloma cell proportion and β2-microglobulin level (P＜0.05),Conclusion The levels of C-reactive protein、hemoglobin and erythrocyte sedimentation rate are closely associated with the development of multiple myeloma. C-reactive protein and hemoglobin are relatively sensitive response to disease than erythrocyte sedimentation rate. There is a clear clinical implication in detecting the patient' s condition for progress and the prognosis.
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Objective To investigate the roles of the chemokine receptor CXCR3 and its ligand I-TAC in the pathogenesis of immune thrombocytopenic purpura (ITP).Methods A total of 48 ITP patients were enrolled in this study:30 with newly diagnosed or relapse ITP and 18 in remission after treatment,and 24 healthy volunteers were as controls.IFNγ and I-TAC in plasma were detected by ELISA.The mRNA expression of CXCR3 in the peripheral blood mononuclear cells (PBMNCs) was determined by quantitative RT-PCR.Results The IFNγ level in the plasma of ITP patients before the treatment was obviously increased than those in the remission group and controls[ (71.45 ± 17.62)ng/L vs (36.94 ±14.86 )ng/L and (25.28 ± 12.85 )ng/L,all P ＜ 0.05 ]and those in the remission group was higher than in the controls ( P ＜ 0.05 ).In contrast,there were no statistic differences of the levels of I-TAC among the three groups[ (455.56 ± 144.70 ) ng/L,( 488.24 ± 164.70 ) ng/L and ( 382.97 ± 167.43 ) ng/L,P ＞0.05 ].Both ITP patients before the treatment and remission groups expressed more CXCR3 mRNA [ 6.76(3.03,37.00),1.76 (0.45,14.18 ) vs 0.12 ( 0.04,0.28 ),P ＜ 0.05 ].After effective therapy,CXCR3mRNA expression decreased,while it was still higher than that in the controls.Conclusions Our data demonstrate that Th1 cytokine (IFNγ) dominance is reflected in ITP.Simultaneously,the CXCR3 + cell may play a role in cell-mediated immunity through chemotaxis in ITP.
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Objective To explore the clinical significance of immunocyte subsets before and after immunosuppressive therapy in the peripheral blood of patients with immune thrombocytopenic purpura (ITP).MethodsThe percentages of immunocyte subsets in the peripheral blood of 35 patients with ITP and 20 healthy controls were detected by flow cytometry,including CD3+,CD4+,CD8+,CD56+,CD19+ lymphocytes and CD4+/CD8+.Results The percentages of CD3+ T lymphocyte (61.58 ± 6.45 ) %,CD4+ T lymphocyte (28.38 ±4.89)% and the ratio of CD4+/CD8+ 0.99 0.22 in patients with ITP were lower than those in healthy controls[( 67.85 ± 4.68 ) %,( 38.00 ± 3.37 ) %,1.54 ± 0.13,all P ＜ 0.05].After immunosuppressive therapy,the percentages of CD3+ T lymphocyte ( 69.41 ± 5.03 ) %,CD4+ T lymphocyte (38.17 ±3.18)% and the ratio of CD4+/CD8+ 1.60 ±0.15 recovered to control levels.The percentages of CD8+ T lymphocyte (29.20 ±4.50)% and CD19+B lymphocyte ( 17.74 ±4.14)% were higher than those in healthy controls[( 24.82 ± 2.93 ) % and ( 12.09 ± 3.51 ) %,all P ＜ 0.05].After the immunosuppressive therapy,the percentages of CD8+ T lymphocyte ( 24.06 ± 3.02 ) % and CD19+ B lymphocyte ( 10.90 ± 3.55 ) %recovered to control levels.There were no significant difference of the percentage of CD56+ lymphocyte among ITP patients ( 15.80 ± 2.85 )%,ITP patients after immunosuppressive therapy ( 15.16 ± 2.77 )% and healthy controls ( 16.36 ± 2.75 ) %.ConclusionThe aberrant immunocyte subsets are involved in the pathogenesis of ITP,and detection of immunocyte subsets might be helpful for the diagnosis and determination of therapeutic outcome of ITP.
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Objective:To measure the nuclear factor kappa B(NF-?B) activation and its mRNA expression in the PBMC,and to analyze the interaction between NF-?B activation and IL-1?,IL-6,TNF-? mRNA expression for exploration the role of NF-?B in production of cytokine in schizophrenia.Methods:Transcription Factor Assay Kits were used to measure NF-?B activation.RT-PCR technique was perftormed to analyze semiquantitatively NF-?B,IL-1?,IL-6 and TNF-? mRNA expression in the PBMC in both schizophrenia and control group.Results:NF-?B activation and its mRNA expression in the schizophrenia group were significantly higher than in the control group(P0.05).IL-1?,IL-6 and TNF-? mRNA expressions in the PBMCs from the schizophrenia group were significantly higher than those from the control subjects(P0.05).Conclusion:It is of significance to measure NF-?B activation in evaluating the regulation function of NF-?B.Activated NF-?B plays an important role in mediating the expression of IL-1? and TNF-? gene in schizophrenia.