Study of recombinant human interleukin-12 for treatment of complications after radiotherapy for tumor patients

AIM To evaluate the treatment effects of recombinant human interleukin-12(rh IL-12) on radiotherapy complications, such as severe myelosuppression or pancytopenia, the decline or imbalance of immune function, etc.METHODS The patients received high-dose and short-course precise radiotherapy, such as Cyber knife and image-guided radiotherapy(IGRT), which can cause myelosuppression or pancytopenia and immune function decline within a short time. One-hundred subjects were enrolled in the study, and 50 were randomized to a treatment group which used rh IL-12 and 50 were randomized to a control group which used symptomatic and supportive therapy after radiotherapy. The 50 subjects in the treatment group were further divided into five subgroups and intervenedwith rh IL-12 at a dose of 50, 100, 150, 200 or 250 ng/kg respectively. The dose-effect relationship was observed. RESULTS Rh IL-12 significantly attenuated the decrease of peripheral blood cells in the treatment group, and immune function was improved after treatment. Due to the different radiation doses, there was a fluctuation within 12 h after treatment but mostly showing an increasing trend. As to the clinical manifestations, 2 patients in the 250 ng/kg subgroup showed low fever after administration, 1 patient in the 200 ng/kg subgroup and 2 patients in the 250 ng/kg subgroup showed mild impairment of liver function during the observation period.CONCLUSION Rh IL-12 has effective therapeutic and protective effects on complications following radiotherapy, such as the decline of blood cells, myelosuppression and the decline or imbalance of immune function, which indicated good prospects for development and application.

Protective effect of recombinant human IL-1Ra on CCl_4-induced acute liver injury in mice

AIM: To evaluate the effects of positive regulation of recombinant human interleukin 1 receptor antagonist (rhIL-1Ra) on hepatic tissue recovery in acute liver injury in mice induced by carbon tetrachloride (CCl 4 ). METHODS: Acute liver damage was induced by injecting 8-wk-old mice with CCl 4 1 mL/kg (1:3 dilution in corn oil) intraperitoneally (ip). Survival after liver failure was assessed by injecting 8-wk-old mice with a lethal dose of CCl 4 2.6 mL/kg (1:1 dilution in corn oil) ip. Mice were subcutaneously injected with 1 mg/kg recombinant human IL-1Ra twice a day after CCl 4 treatment for 5 d. Serum alanine amino transferase (ALT) and aspartate aminotransferase (AST) levels were determined with a commercial assay kit. Serum IL-1β, IL-1Ra levels were measured by enzyme-linked immunosorbent assay kit. Quantitative real-time polymerase chain reaction was used to determine liver IL-1β, IL-1Ra and IL-6 expression during CCl 4-induced acute liver injury. Liver sections were stained with hematoxylin-eosin. A histology-injury grading system was used to evaluate the degree of necrosis after acute liver injury. Proliferating cell nuclear antigen (PCNA) staining was used to evaluate the role of rhIL-1Ra in promoting hepatocyte proliferation. RESULTS: Quantitative analysis showed a higher level of IL-6 mRNA expression and reduced serum AST and ALT levels in the livers of the rhIL-1Ra-treated group at the early phase of CCl 4-induced acute liver injury. Histological examination indicated a decrease in centrilobular necrotic areas in mice treated with rhIL-1Ra, and a novel role of rhIL-1Ra in promoting hepatocyte proliferation was also supported by an increase of PCNA staining. All these results, accompanied by a strong survival benefit in rhIL-1Ra-treated vs PBS-treated groups, demonstrated that rhIL-1Ra administration ameliorated the histological damage and accelerated the regeneration and recovery process of the liver. CONCLUSION: rhIL-1Ra could be further developed as a novel therapeutic agent for the treatment of acute liver injury because of its ability to reduce hepatocellular damage and facilitate liver regeneration.

Construction of Saccharomyces cerevisiae Strain Stably Expressing a Fusion Protein Containing Ten Tandem Recombinant Human Glucagon-like Peptide-1 Analogues

The recombinant Saccharomyces cerevisiae strain stably expressing recombinant human glucagon-like peptide-l（rhGLP-1） analogue, as a potential oral drug delivery system for diabetes type II treatment, was successfully constructed by the homologous recombination between chromosomal DNA and yeast and integrating vector pNK-GLP containing yeast ribosomal DNA fragments. The amount of rhGLP-I analogue fusion protein in transformant SG2 reached ca. 0.84 mg per gram of packed cells when SG2 was grown for 24 h in the YPD medium with a inoculum and medium ratio of 1：1. Oral administration of 5 g lyophilized SG2/kg to hyperglycemic rats decreased serum glucose from （24.8±1.40） to （21.2±1.36） mmol/L.

Efficacy of recombinant human osteoprotegerin combined with tinidazole in the treatment of periodontitis mice and its correlation with serum RANKL and MCP-1 levels

Objective: To investigate the effect of recombinant human osteoprotegerin combined with tinidazole on mice with periodontitis and the effect on serum RANKL and MCP-1 levels. Methods: 80 SPF-cleaned mice were randomly divided into 4 groups, 20 each, model group, tinidazole group and recombinant human osteoprotegerin group were modeled by Kimura et al., and tinidazole group received tinidazole. After intragastric administration, the recombinant human osteoprotegerin group was injected with recombinant human osteoprotegerin in the periodontal pocket according to the tinidazole group. The periodontal changes of the four groups of mice were observed and recorded, and the gingival rating was performed. Epithelial tissue morphology was observed by hematoxylin-eosin (HE) staining. Serum levels of IL-4, IL-6, RANKL and MCP-1 were measured by enzyme-linked immunosorbent assay. Results:After the intervention, the model group developed severe inflammatory reactions, including redness, hemorrhage, and deep periodontal pockets. The teeth were significantly loosened. The mice in the tinidazole group and the recombinant human osteoprotegerin group recovered substantially, and the gingival rating of the recombinant human osteoprotegerin group was better than that. The tinidazole group and the model group (P<0.05). The results of HE staining showed that the model group had edema, vasodilation and a large amount of inflammatory infiltration. The epithelial structure of the mice in the tinidazole group and the recombinant human osteoprotegerin group was intact and arranged closely and orderly. After intervention, the IL-4 in the tinidazole group and the recombinant human osteoprotegerin group was significantly higher than the model group and IL-6 was significantly lower than the model group (P<0.05), and the recombinant human osteoprotegerin group IL-4 was significantly higher after the intervention. IL-6 was significantly lower in the tinidazole group than in the tinidazole group (P<0.05). After the intervention, the tinidazole group and the recombinant human osteoprotegerin group were significantly reduced, and the recombinant human osteoprotegerin group RAKNL and MCP-1 were significantly lower than the model group (P>0.05). Conclusion: Recombinant human osteoprotegerin combined with tinidazole has a better therapeutic effect on gums and teeth in mice with periodontitis, and can lower the levels of RAKNL and MCP-1 in serum, inhibit bone resorption and protect teeth.

Effects of systemic domestic recombinant human erythropoietin on HIF-1α expression in the retina in a rabbit model of acute high intraocular pressure

Objective To observe the expression of hypoxia inducible factor-1α (HIF-1α) in the retina of rabbits with acute high intraocular pressure and to investigate the mechanism of systemic domestic recombinant human erythropoietin (rhEPO) protecting the retina from ischemia-reperfusion injury. Methods First,control group and model group were established in rabbit eyes. The acute high intraocular pressure model was established by saline perfusion into anterior chamber,and then hypodermic injection of domestic rhEPO was made. HIF-1α protein in the retina was observed by immunohistochemical staining method on days 1,3,7 and 14 after retinal ischemia-reperfusion,respectively. Results No cells with HIF-1α positive expression were observed in the retina of the control group. Cells with HIF-1α positive expression in the model group outnumbered those in the control group (P<0.01). The resemblance pattern occurred in EPO group but its degree was slightly greater than that in the model group from day 3 after ischemia-reperfusion (P<0.05). Conclusion Domestic rhEPO can down-regulate the expression of HIF-1α in the retina with acute high intraocular pressure,which may be one of the mechanisms that rhEPO protects the retina from ischemia-reperfusion injury.

Neuronal changes in the retinal ganglion cell layer following recombinant human interleukin-2 intravitreal injection in a rat model of chronically elevated intraocular pressure

Intraperitoneal injection of recombinant human interleukin-2（rhIL-2）inhibits neuronal apoptosis in the chronic ocular hypertension retinal ganglion cell layer.Intravitreous injection was performed on retinal ganglion cells in a Wistar rat model of chronically elevated intraocular pressure to observe the effects of LY294002 and AG490 on retinal ganglion cell survival,macrophage activation,and PI3K/Akt and JAK/STAT activation.The number of retinal ganglion cells in the rhIL-2 treatment group was much greater than in the normal control and phosphate-buffered saline groups.Western blot analysis revealed low Akt and STAT3 protein expression in the retina after 3-hour intravitreous injections of rhIL-2.However,protein expression was increased at 12 hours,but decreased again at 24 hours,with very low expression at 96 hours.LY294002 and AG490,which are inhibitors of the PI3K/Akt and JAK/STAT3 signal pathways,prevented upregulation of Akt and STAT3 protein expression in the retina,respectively.Intravitreous injection of rhIL-2 exhibited neuroprotective effects by decreasing retinal ganglion cell layer damage in a rat model of chronic glaucoma.These results suggest that intravitreal injection of rhIL-2 could induce the PI3K/Akt and JAK/STAT3 signaling pathways to protect retinal ganglion cells in chronically elevated intraocular pressure models.

The Concept Study of Recombinant Human Soluble Thrombomodulin in Patients with Acute Respiratory Distress Syndrome

Background: Recombinant human soluble thrombomodulin (rhTM) was approved for the treatment of disseminated intravascular coagulation in Japan, and rhTM has anti-inflammatory effects. Disordered coagulation is a part of the acute respiratory distress syndrome (ARDS) pathophysiology and thus we hypothesize that anticoagulant therapy may help. This preliminary study was to observe the safety of rhTM administration and the improvement on biomarker levels after the therapy for ARDS-patients. Objectives: Case series of ARDS-patients. Methods: Seventeen ARDS-patients that required ventilatory management were treated with rhTM and clinical and laboratory data were collected including platelets, thrombin-antithrombin complex (TAT), fibrinogen degradation products, oxygen saturation/the fraction of inspired oxygen (SpO2/FIO2), and high-mobility group-1 (HMG-1). The administration of rhTM was started during 6 days at a bolus dose of 0.06 mg/kg/day immediately after the diagnosis of ARDS. Results: Eleven of the 17 ARDS-patients were alive at 28 days after the beginning of the administration of rhTM. The serial pattern of the SpO2/FIO2 showed remarkable differences between the survivors and nonsurvivors from day 5 to day 7. The TAT in the survivors significantly decreased after treatment, and there were significantly lower levels in the TAT on day 7 in comparison to that of the nonsurvivors. The serial changes of HMG-1 showed increased levels in the nonsurvivors until day 5 after the administration of rhTM. Conclusions: Additional rhTM administration can safely improve the parameters in survival ARDS-patients, as demonstrated by significant improvements in the SpO2/FIO2, HMG-1 and TAT.

Upregulation of stromal cell-derived factor-1 alpha/CXCR4 axis-induced migration of human neural progenitors by tumor necrosis factor-alpha and interleukin-8

BACKGROUND： Studies of several animal models of central nervous system diseases have shown that neural progenitor cells （NPCs） can migrate to injured tissues. Stromal cell-derived factor 1 alpha （SDF-la）, and its primary physiological receptor CXCR4, have been shown to contribute to this process. OBJECTIVE： To investigate migration efficacy of human NPCs toward a SDF-1α gradient, and the regulatory roles of tumor necrosis factor-α （TNF-α） and interleukin-8 （IL-8） in SDF-1α/CXCR4 axis-induced migration of NPCs. DESIGN, TIME AND SETTING： An in vitro, randomized, controlled, cellular and molecular biology study was performed at the Laboratory of Department of Cell Biology, Medical College of Soochow University between October 2005 and November 2007. MATERIALS： SDF-1α and mouse anti-human CXCR4 fusion antibody were purchased from R＆D Systems, USA. TNF-αwas purchased from Biomyx Technology, USA and IL-8 was kindly provided by the Biotechnology Research Institute of Soochow University. METHODS： NPCs isolated from forebrain tissue of 9 to 10-week-old human fetuses were cultured in vitro. The cells were incubated with 0, 20, and 40 ng/mL TNF-α, or 0, 20, and 40 ng/mL IL-8, for 48 hours prior to migration assay. For antibody-blocking experiments, cells were further pretreated with 0, 20, and 40 μg/mL mouse anti-human CXCR4 fusion antibody for 2 hours. Subsequently, the transwell assay and CXCR4 blockade experiments were performed to evaluate migration of human NPCs toward a SDF-1α gradient. Serum-free culture medium without SDF-1α served as the negative control. MAIN OUTCOME MEASURES： The transwell assay was performed to evaluate migration of human NPCs toward a SDF-1α gradient, which was blocked by fusion antibody against CXCR4. In addition, CXCR4 expression in human NPCs stimulated by TNF-α and IL-8 was measured by flow cytometry. RESULTS： Results from the transwell assay demonstrated that SDF-1α was a strong chemoattractant for human NPCs （P 〈 0.01）, and 20 ng/mL produced the highest levels of migration. Anti-human CXCR4 fusion antibody significantly blocked the chemotactic effect （P 〈 0.05）. Flow cytometry results showed that treatment with TNF-α and IL-8 resulted in increased CXCR4 expression and greater chemotaxis efficiency of NPCs towards SDF-1α（P 〈 0.01）. CONCLUSION： These results demonstrated that SDF-la significantly attracted NPCs in vitro, and neutralizing anti-CXCR4 antibody could block part of this chemotactic function. TNF-α and IL-8 increased chemotaxis efficiency of NPCs towards the SDF-1αgradient by upregulating CXCR4 expression in NPCs.

IL-1β通过激活ERK1/2信号通路抑制人脐带间充质干细胞CD200表达抑制巨噬细胞M2极化

目的探究白细胞介素1β(IL-1β)调控人脐带间充质干细胞CD200表达及其对巨噬细胞极化的影响及作用机制。方法无血清培养基分离培养获得人脐带间充质干细胞(hUC-MSC),形态学观察及流式细胞术检测CD73、CD90、CD105、CD14、CD34、CD45、人类白细胞抗原DR(HLA-DR)的表达,确定间充质干细胞属性;20 ng/mL IL-1β处理hUC-MSC 24 h,流式细胞术检测CD200阳性细胞率,实时定量PCR和Western blot法检测CD200 mRNA和蛋白表达水平;佛波酯(PMA)诱导THP-1巨噬细胞活化,并与IL-1β处理感染CD200过表达慢病毒的hUC-MSC共培养,流式细胞术检测CD11c和CD206阳性细胞比例;IL-1β联合细胞外信号调节激酶1/2(ERK1/2)特异性抑制剂PD98059处理hUC-MSC,Western blot法检测细胞丝裂原激活蛋白激酶(MAPK)信号分子与CD200的表达。结果IL-1β显著下调hUC-MSC CD200蛋白表达与CD200阳性细胞率;过表达CD200显著上调hUC-MSC CD200表达,且CD200过表达hUC-MSC提高巨噬细胞CD206阳性细胞比率;IL-1β激活hUC-MSC的ERK1/2信号通路,PD98059上调IL-1β处理后hUC-MSC中CD200的蛋白表达。结论IL-1β通过激活ERK1/2信号通路抑制CD200的表达,进而抑制hUC-MSC对巨噬细胞向M2型极化的促进作用。

TP患者应用IL-11联合重组人血小板生成素治疗的临床疗效及安全性

目的:探讨血小板减少症(TP)患者应用白细胞介素(IL)-11联合重组人血小板生成素注射液治疗的临床疗效及安全性。方法:选取2022年8月至2023年8月在漯河医学高等专科学校第二附属医院接受治疗的150例TP患者,随机均分为常规组与联合组,每组各纳入75例。常规组给予应用IL-11治疗,联合组在常规组的基础上联合应用重组人血小板生成素输注治疗。观察两组患者治疗期间血小板计数的变化,比较血小板计数达标时间;治疗14 d,观察血清学检测指标的变化;出院前统计两组患者不良反应发生情况并比较。结果:治疗3 d、7 d、14 d时,联合组患者血小板计数均高于常规组;联合组患者血小板计数恢复至≥50×10^(9)·L^(-1)时间、≥70×10^(9)·L^(-1)时间、≥100×10^(9)·L^(-1)时间均短于常规组;治疗14 d时,联合组血清促血小板生成素(TPO)、IL-6、肿瘤坏死因子-α(TNF-α)水平均低于常规组,差异均具有统计学意义(P<0.05)。两组患者不良反应总发生率的差异无统计学意义(P>0.05)。结论:IL-11联合重组人血小板生素注射液治疗TP可获得理想的临床疗效,能有效缩短血小板达标时间,且联合方案安全性可靠。

羧甲司坦口服溶液联合重组人干扰素α1b治疗小儿急性喘息性支气管炎的效果

目的分析急性喘息性支气管炎患儿接受重组人干扰素α1b单药与联合羧甲司坦口服溶液治疗的效果。方法回顾性分析2021年6月至2023年6月医院收治的100例急性喘息性支气管炎患儿资料,按不同治疗方案分为对照组、观察组,各50例。对照组接受重组人干扰素α1b治疗,观察组接受羧甲司坦口服溶液联合重组人干扰素α1b治疗。比较两组临床疗效、主要症状缓解时间、气道炎症相关因子[趋化因子配体3(CCL3)、高迁移率族蛋白B1(HMGB1)、α1-酸性糖蛋白(α1-AG)]、T淋巴细胞(CD3^(+)、CD4^(+)、CD4^(+)/CD8^(+))及不良反应。结果观察组临床总有效率高于对照组(P<0.05)。治疗后观察组气促、喘息、咳嗽、肺部音等症状缓解时间降低(P<0.05)。治疗4、7 d后,两组CCL3、HMGB1、α1-AG较治疗前下降,且观察组低于对照组(P<0.05);两组CD3^(+)、CD4^(+)、CD4^(+)/CD8^(+)较治疗前升高,且观察组高于对照组(P<0.05)。两组不良反应发生率比较,差异无统计学意义(P>0.05)。结论羧甲司坦口服溶液联合重组人干扰素α1b治疗急性喘息性支气管炎,可抑制气道炎症,调节机体免疫,促进症状缓解,疗效确切,且安全性高。

Why interleukin-10 supplementation does not work in Crohn's disease patients

Inflammatory bowel diseases (IBD) such as Crohn's disease (CD) or ulcerative colitis are chronic intestina disorders, which are on the increase in "Westernised" countries. IBD can be caused by both genetic and environmental factors. Interleukin-10 (IL-10) is an immunoregulatory cytokine that has been identified as being involved in several diseases including IBD. Studies have shown that polymorphisms in the promoter region reduce serum levels of IL-10 and this reduction has been associated with some forms of IBD. Mouse models have shown promising results with IL-10 supplementation, as such IL-10 supplementation has been touted as being a possible alternative treatment for CD in humans. Clinical trials have shown that recombinant human IL-10 is safe and well tolerated up to a dose o 8 μg/kg. However, to date, the results of the clinica trials have been disappointing. Although CD activity was reduced as measured by the CD activity index IL-10 supplementation did not result in significantly reduced remission rates or clinical improvements when compared to placebo. This review discusses why IL-10supplementation is not effective in CD patients currently and what can be addressed to potentially make IL-10 supplementation a more viable treatment option in the future. Based on the current research we conclude that IL-10 supplementation is not a one size fits all treatment and if the correct population of patients is chosen then IL-10 supplementation could be of benefit.

Effects of adenoviral vector-mediated transduction of human p53,B7-1 and GM-CSF genes on liver cancer cells

The potential efficacy and clinical feasibility of gene therapy for liver cancer were tested through therecombinant adenovirus-mediated (Ad-multigenes ) co-transfer of human wild-type p53, B7-l co-stimulation(CD8o) and granulocyte-macrophage colony-stimulating factor (GM-CSF) genes into human hepatocellular carcinoma cell lines. The treated cells underwent apoptosis with specific DNA fragmentation and became more sensitiveto cisplatin, a chemotherapeutic drug. Their growth was partly inhibited. Efficient proliferation and generation ofCTLs and cytokine production were induced in mixed lymphocytes through tumor cell reaction (MLTR) using peripheral blood T lymphocytes from donors as effector cells and Ad-multigenes or Ad-p53-transfected human hepatocellular carcinoma cells (HepG2 or BEL7402) as stimulator cells. Ad-multigenes-transfected rat carcinosarcomaWalker 256 cells were inoculated subcutaneously into normal rats. Fourteen days later, the activity of spleen cellsin rats inoculated with Ad-multigenes-transduced Walker 256 cells was higher than that in Ad-p53-transducedones. These findings suggest that adenovirus-mediated multigenes p53, B7-1 and GM-CSF can induce apoptosis ofliver cancer cells and initiate a potent antitumor immune response against them.

Caspase-1 activation and mature interleukin-1β release are uncoupled events in monocytes

AIM:To investigate whether caspase-1 activation/intracellular processing of pro-interleukin-1β(pro-IL-1β) and extracellular release of mature IL-1β from activated monocytes are separable events.METHODS:All experiments were performed on fresh or overnight cultured human peripheral blood monocytes(PBMCs) that were isolated from healthy donors.PBMCs were activated by lipopolysaccharide(LPS) stimulation before being treated with Adenosine triphosphate(ATP,1 mmol/L),human α-defensin-5(HD-5,50 μg/mL),and/or nigericin(Nig,30 μmol/L).For each experiment,the culture supernatants were collected separately from the cells.Cell lysates and supernatants were both subject to immunoprecipitation with anti-IL1β antibodies followed by western blot analysis with anti-caspase-1 and anti-IL-1β antibodies.RESULTS:We found that pro-IL-1β was processed to mature IL-1β in LPS-activated fresh and overnight cultured human monocytes in response to ATP stimulation.In the presence of HD-5,this release of IL-1β,but not the processing of pro-IL-1β to IL-1β,was completely inhibited.Similarly,in the presence of HD-5,the release of IL-1β,but not the processing of IL-1β,was significantly inhibited from LPS-activated monocytes stimulated with Nig.Finally,we treated LPS-activated monocytes with ATP and Nig and collected the supernatants.We found that both ATP and Nig stimulation could activate and release cleaved caspase-1 from the monocytes.Interestingly,and contrary to IL-1β processing and release,caspase-1 cleavage and release was not blocked by HD-5.All images are representative of three independent experiments.CONCLUSION:These data suggest that caspase-1 activation/processing of pro-IL-1β by caspase-1 and the release of mature IL-1β from human monocytes are distinct and separable events.

重组人生长激素治疗对身材矮小症患儿血清IGF-1、Ghrelin及LP水平的影响

目的探讨重组人生长激素(rhGH)治疗对身材矮小症患儿的疗效及其对血清胰岛素样生长因子-1(IGF-1)、饥饿激素(Ghrelin)及瘦素(LP)水平的影响。方法选择该院2021年1—12月收治的身材矮小症患儿79例为研究对象,按照随机数字表法将其分为对照组39例和观察组40例。对照组采用加强营养,并补充钙质、微量元素和各种维生素等常规治疗,观察组在常规治疗的基础上给予rhGH治疗,两组治疗时间均为12个月。比较两组患儿治疗前和治疗12个月后身高、生长速度、身高标准差积分(HtSDS)及血清IGF-1、Ghrelin、LP水平变化,比较两组不良反应发生情况。结果治疗前,两组患儿身高、生长速度、HtSDS及血清IGF-1、Ghrelin、LP水平比较,差异均无统计学意义(P>0.05);治疗12个月后,两组患儿身高、HtSDS及血清IGF-1、LP水平均高于治疗前,生长速度均快于治疗前,血清Ghrelin水平均低于治疗前,差异均有统计学意义(P<0.05);观察组患儿治疗12个月后身高、HtSDS及血清IGF-1、LP水平均高于对照组,生长速度快于对照组,血清Ghrelin水平低于对照组,差异均有统计学意义(P<0.05);对照组患儿治疗期间未出现任何不良反应,观察组治疗期间出现甲状腺功能减退1例,膝部疼痛2例,但两组患儿不良反应发生率比较,差异无统计学意义(P>0.05)。结论rhGH可有效改善身材矮小症患儿血清IGF-1、Ghrelin及LP水平,促进患儿生长,临床疗效满意,安全性高,值得临床应用。

ApoA-1表达与重组人脑钠肽治疗急性心肌梗死的不良心血管事件相关性分析

目的研究血浆载脂蛋白A-1(ApoA-1)表达与重组人脑钠肽治疗急性心肌梗死(AMI)的不良心血管事件相关性。方法回顾性分析2021年3月至2023年2月于陕西中医药大学第二附属医院心内科进行重组人脑钠肽治疗的AMI患者132例,根据是否发生不良心血管事件分为发生组(n=19)和未发生组(n=113)。从脑卒中、心源性死亡、再发性心肌梗死、心绞痛发作四种结局分别分析与ApoA-1表达的相关性。对AMI患者重组人脑钠肽治疗后发生不良心血管事件进行单因素、多因素Logistic回归分析,探究ApoA-1表达水平与重组人脑钠肽治疗AMI的不良心血管事件相关性。结果与发生组相比,未发生组ApoA-1表达水平更高,具有统计学差异(P<0.05);与发生组相比,未发生组左心室收缩末期内径(LVESD)、左心室舒张末期内径(LVEDD)、血肌酐(SCr)、尿素氮(BUN)水平降低,左心室射血分数(LVEF)、肾小球滤过率(eGFR)水平均升高,具有统计学差异(P<0.05)。心源性死亡组、再发性心肌梗死组、脑卒中组、心绞痛发作组的ApoA-1水平明显低于不良心血管事件未发生组,各亚组间的脂质代谢指标均具有统计学差异(P<0.05)。Logistic回归分析显示,空腹血糖(FBG)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、ApoA-1水平变化是影响AMI患者重组人脑钠肽治疗后发生心源性死亡、再发性心肌梗死、脑卒中、心绞痛发作的危险因素,具有统计学差异(P<0.05)。通过Pearson分析得出,ApoA-1表达与重组人脑钠肽治疗AMI的心源性死亡、再发心肌梗死、脑卒中、心绞痛发作不良心血管事件均呈正相关,具有统计学差异(P<0.05)。结论ApoA-1表达水平异常是造成AMI患者进行重组人脑钠肽治疗后发生不良心血管事件的危险因素。

不同剂量重组人生长激素对特发性矮小症患儿25-羟维生素D、胰岛素样生长因子1水平的影响

目的分析不同剂量重组人生长激素(rhGH)对特发性矮小症(ISS)患儿25-羟维生素D、胰岛素样生长因子1(IGF-1)水平的影响。方法选取2019年12月至2021年7月在山东大学附属儿童医院儿童保健所就诊的ISS儿童共72例为研究对象。患儿均在常规营养支持治疗基础上给予rhGH治疗,根据rhGH的剂量不同分为两组,对照组(34例)的剂量为0.15IU/(kg·d),观察组(38例)的剂量为0.20 IU/(kg·d),比较两组身高、身高标准差积分(HtSDS)、体重指数(BMI)及治疗后25-羟维生素D、IGF-1水平的变化。结果两组治疗前身高、HtSDS、BMI、25-羟维生素D、IGF-1水平比较,差异无统计学意义(P>0.05);治疗后,观察组HtSDS、IGF-1水平均高于对照组(P<0.05)。结论高剂量rhGH可有效改善ISS儿童的身高及IGF-1水平,值得临床应用。

聚乙二醇重组人生长激素对特发性矮小症患儿胰岛素样生长因子-1水平的影响

目的分析评估不同剂量聚乙二醇重组人生长激素对治疗特发性矮小症患儿胰岛素样生长因子-1水平的影响。方法随机选取2020年6月至2023年6月福建医科大学附属第二医院收治的80例特发性矮小症患儿进行回顾性分析,将其按照使用聚乙二醇重组人生长激素的不同剂量分为对照组和观察组,每组各40例。其中,对照组的40例特发性矮小症患儿采取小剂量进行治疗,观察组的40例特发性矮小症患儿则采取0.2 U/(kg·d)进行治疗。比较评估两组患者的临床治疗效果、血糖控制情况、血清IGF-1、IGFBP-3水平、生长情况相关指标、骨代谢相关指标以及不良反应发生情况。结果观察组空腹血糖、餐后2 h血糖低于对照组(P<0.05);观察组血清IGF-1、血清IGFBP-3高于对照组(P<0.05);观察组生长速度、骨龄、身高标准差高于对照组(P<0.05);观察组碱性磷酸酶、血清钙、血清磷指标高于对照组(P<0.05);在不良反应发生情况方面,观察组与对照组之间的数据比较无明显差异(P>0.05)。结论0.2 U/(kg·d)聚乙二醇重组人生长激素在促进特发性矮小症患儿的成长、骨骼功能水平提升以及血清IGF-1和IGFBP-3水平的改善方面均具有比小剂量药物治疗更加显著的治疗效果,并且无额外的不良反应,安全可靠。

社区获得性肺炎患者血清HBD-1、SAA、sIL-2R水平变化及指导病情分级的意义

目的检测社区获得性肺炎(CAP)患者血清防御素-1(HBD-1)、淀粉样蛋白A(SAA)、可溶性白细胞介素-2受体(sIL-2R)水平变化,并分析其对病情分级的指导意义。方法选取2021年7月至2023年8月在该院收治的85例CAP患者(CAP组),根据肺炎严重度指数(PSI)将其分为低风险组(34例)、中风险组(41例)和高风险组(10例),另取85例健康成人作为对照组。比较CAP组和对照组血清HBD-1、SAA和sIL-2R水平,比较PSI不同风险分组血清HBD-1、SAA和sIL-2R水平;采用受试者操作特征(ROC)曲线分析HBD-1、SAA、sIL-2R水平对CAP患者的诊断价值;采用Spearman相关性分析CAP患者PSI值和血清HBD-1、SAA、sIL-2R水平之间的关系。结果CAP患者血清HBD-1、SAA和sIL-2R水平均高于对照组,其中PSI评分不同分组血清HBD-1、SAA和sIL-2R水平由高到低为高风险组>中风险组>低风险组,差异有统计学意义(P<0.05)。ROC曲线分析结果显示,血清HBD-1[曲线下面积(AUC)=0.739]、SAA(AUC=0.773)、sIL-2R(AUC=0.730)水平对CAP患者具有良好的诊断价值(P<0.05)。Spearman相关性分析结果显示,血清HBD-1水平[相关系数(r)=0.304]、SAA(r=0.498)和sIL-2R(r=0.435)水平与PSI评分呈正相关(P<0.05)。结论血清HBD-1、SAA、sIL-2R水平对CAP患者的病情分级具有较好的指导意义。

重组人白介素-11联合生血宝合剂治疗乳腺癌药源性血小板减少症的效果

目的:探讨重组人白介素-11联合生血宝合剂治疗乳腺癌药源性血小板减少症的效果。方法:选取2021年10月—2023年10月赣州市肿瘤医院收治的60例乳腺癌患者,以随机数字表法分为对照组、观察组,各30例。两组患者均接受恩美曲妥珠单抗治疗,对照组给予重组人白介素-11,观察组给予重组人白介素-11联合生血宝合剂。对比两组临床疗效、中医症候、血小板相关指标、治疗安全性。结果:观察组总有效率高于对照组,差异有统计学意义(P<0.05)。治疗后,观察组中医症候积分均低于对照组,差异均有统计学意义(P<0.05)。治疗后,观察组血小板相关指标均高于对照组,差异均有统计学意义(P<0.05)。两组不良反应发生率比较,差异无统计学意义(P>0.05)。结论:重组人白介素-11与生血宝合剂联合治疗乳腺癌药源性血小板减少症的效果良好,可改善患者中医症候,提高血小板计数水平,治疗安全性良好。