A Budd-Chiari Syndrome Due to C Protein Deficiency: A Case Report at YaoundéGeneral Hospital (Cameroon)

Primary Budd-Chiari syndrome (BCS) is a spontaneously fatal disease characterized by an obstruction of the hepatic venous outflow tract due to thrombosis or a primary disease of the venous wall. The primary form of BCS is extremely rare. This is a disease mainly affecting young adults of both sexes. Clinical manifestations are variable;they can be asymptomatic, acute, or subacute but mostly chronic. Several causes have been identified, such as myeloproliferative syndrome, antiphospholipid syndrome, paroxysmal nocturnal hemoglobinuria, and inherited thrombotic disorders. Data on primary BCS in Sub-Saharan Africa is rare as most publications available are case reports. In these reports, the causes are unknown with poor prognosis in most cases often leading to patient death. We herein present a case report of a male patient diagnosed with a primary BCS at Yaoundé General Hospital (Cameroon) caused by a Protein C deficiency who presented with ascites decompensating liver cirrhosis. Treatment was based on anticoagulants, diuretics and laxatives administration. Two years after the diagnosis, the patient is alive with clinical and paraclinical improvement.

Expressions of beta-catenin, APC Protein, C-myc and Cyclin D1 in Ovarian Epithelial Tumor and Their Implication

Objective： To investigate the expressions of beta-catenin, protein APC （adenomatous polyposis coil protein）, c-myc and cyclin D1 and their implication in ovarian epithelial tumor. Methods： Immunohistochemical staining with SP method was conducted to identify the expressions of beta-catenin, APC protein, c-myc and cyclin D1 in ovarian epithelial tumor in 48 cases. Results： The abnormal expression rate of beta-catenin in malignant and borderline ovarian epithelial tumors was higher than that in benign epithelial tumors （P〈0.01）. The expression rates of c-myc and cyclin-D1 in ovarian malignant and borderline epithelial tumors were higher than those in benign epithelial tumors too（P〈0.05）. The prevalence of APC protein positive expression in benign epithelial tumors were significantly greater than that in malignant epithelial tumors （P〈0.05）. A significant negative correlation was found between beta-catenin and APC protein in ovarian epithelial tumors; while a significant positive correlation was found between beta-catenin, c-myc and cyclin-D1 in ovarian epithelial tumor （P〈0.05）. Conclusion： The abnormal expressions of Beta-catenin, APC protein, c-myc and cyclin-D1 might be used to indicate the malignance transform of ovarian epithelial tumors.

VARIATION AND SIGNIFICANCE OF C-MYC PROTEIN IN RAT CARDIAC VOLUME-OVERLOAD HYPERTROPHY

Objective To investigate the change of c-myc protein, which was chosen as the response indicator to volume-overload. Methods The time and spatial course of c-myc protein expression on the model of rat cardiac volume-overload hypertrophy was examined by immunohistochemical study. Results The immunohistochemical study indicated the expression of c-myc protein was increased obviously at 4-6 hours (62.73%) than that of control (45.41%, P<0.01) after the volume-overload, then decreased gradually along with development of volume-overload hypertrophy and was decreased extremely at 5 months(r=-0.514,P<0.01).Conclusion There are disorders in the signal transduction pathways governing the hypertrophic response of cardiomyocytes in hypertrophic myocardium. C-myc gene and the product of it may be only the promoter gene of myocardial hypertrophy. Once switching on,c-myc gene and the product of it do not act anymore;While it may be that c-myc gene and the product of it increased following with myocardial hypertrophy, and have not direct relation to the occurrence and development of myocardial hypertrophy.

Regulations of Thyroid Hormone on Cardiac Protein Kinase C Signal Pathway in vitro

The experiments were conducted to assess the influences of thyroid hormone on cardiac protein kinase C(PKC) signal pathway with cultured cardiac myocytes and fibroblasts as the models. Cells were pretreated with 1% newborn calf serum (NCS) or angiotensin II (Ang II), and then following by a triiodothyronine (T3) treatment. The PKC activity, PKCα and PKCε expressions were analyzed and compared. In 1% NCS pretreatment, T3 could inhibit PKC activity and PKCε expression in cardiac myocytes. The AngII pretreatment led to an increase of PKC activity and PKCε expression in cardiac myocytes, and an increase of PKC activity in cardiac fibroblasts. Following by T3 treatment, the increased PKC activity and PKCε expression in cardiac myocytes were markedly decreased. In conclusion, whether in 1% NCS or in Ang II pretreatment, T3 could inhibit PKC activity and PKCε expression in cardiac myocytes. Key words thyroid hormone - cardiac myocytes - cardiac fibroblasts - protein kinase C CLC number Q 572 Foundation item: Supported by the Natural Science Foundation of Hubei Province (98091)Biography: WANG Bao-hua (1974-), female, Ph. D, research direction: cardiovascular pathophysiology.

Exogenous bone morphogenetic protein-7 reduces hepatic fibrosis inSchistosoma japonicum-infected micevia transforming growth factor-β/Smad signaling

AIM: To investigate the antifibrotic effects of bone morphogenetic protein-7 (BMP-7) on Schistosoma japonicum (S. japonicum )-induced hepatic fibrosis in BALB/C mice. METHODS: Sixty BALB/C mice were randomly divided into three groups, including a control group (group A, n = 20), model group (group B, n = 20) and BMP-7 treated group (group C, n = 20). The mice in group B and group C were abdominally infected with S. japonicum cercariae to induce a schistosomal hepatic fibrosis model. The mice in group C were administered human recombinant BMP-7. Liver samples were extracted from mice sacrificed at 9 and 15 wk after modeling. Hepatic histopathological changes were assessed using Masson's staining. Transforming growth factor-beta 1 (TGF-β1), alpha-smooth muscle actin (α-SMA), phosphorylated Smad2/3 (pSmad2/3) and Smad7 protein levels and localization were measured by Western blotting and immunohistochemistry, respectively, and their mRNA expressions were detected by reverse transcriptionpolymerase chain reaction (RT-PCR). RESULTS: The schistosomal hepatic fibrosis mouse model was successfully established, as the livers of mice in group B and group C showed varying degrees of typical schistosomal hepatopathologic changes such as egg granuloma and collagen deposition. The degree of collagen deposition in group C was higher than that in group A (week 9: 22.95±6.66vs 2.02±0.76; week 15: 12.84±4.36 vs 1.74±0.80; P<0.05), but significantly lower than that in group B (week 9: 22.95±6.66 vs 34.43±6.96; week 15: 12.84±4.36 vs 18.90±5.07;P<0.05) at both time points. According to immunohistochemistry data, the expressions of α-SMA, TGF-β1 and pSmad2/3 protein in group C were higher than those in group A (α-SMA: week 9: 21.24±5.73 vs 0.33±0.20; week 15: 12.42±4.88 vs 0.34±0.27; TGF-β1: week 9: 37.00±13.74 vs 3.73±2.14; week 15: 16.71±9.80 vs 3.08±2.35; pSmad2/3: week 9: 12.92±4.81 vs 0.83±0.48; week 15: 7.87±4.09 vs 0.90±0.45; P<0.05), but significantly lower than those in group B (α-SMA: week 9: 21.24±5.73 vs 34.39±5.74; week 15: 12.42±4.88 vs 25.90±7.01; TGF-β1: week 9: 37.00±13.74 vs 55.66±14.88; week 15: 16.71±9.80 vs 37.10±12.51; pSmad2/3: week 9: 12.92±4.81 vs 19.41±6.87; week 15: 7.87±4.09vs 13.00±4.98;P<0.05) at both time points; the expression of Smad7 protein in group B was higher than that in group A and group C at week 9 (8.46±3.95 vs 1.00±0.40 and 8.46±3.95 vs 0.77±0.42; P<0.05), while there were no differences in Smad7 expression between the three groups at week 15 (1.09±0.38 vs 0.97±0.42 vs 0.89±0.39; P>0.05). Although minor discrepancies were observed, the results of RT-PCR and Western blotting were mainly consistentwith the immunohistochemical results. CONCLUSION: Exogenous BMP-7 significantly decreased the degree of hepatic fibrosis in both the acute and chronic stages of hepato-schistosomiasis, and the regulatory mechanism may involve the TGF-β/Smad signaling pathway.

C反应蛋白/白蛋白比值对2型糖尿病合并急性心肌梗死患者远期不良心脑血管事件的预测价值研究

背景急性心肌梗死(AMI)是威胁全球公众健康的主要原因之一。虽然已有相应的再灌注治疗策略,但AMI相关的主要不良心脑血管事件(MACCEs)仍然是全世界人口死亡的原因之一。尤其合并糖尿病的AMI患者,因冠状动脉病变复杂,病变程度严重,尽早发现和判断该部分患者远期预后相对困难,因此寻找相对简便、易获得的实验室指标,有利于为2型糖尿病(T2DM)合并AMI患者经皮冠状动脉介入(PCI)术后MACCEs的预测提供依据。目的探讨血清C反应蛋白(CRP)/白蛋白(Alb)比值(CAR)对T2DM合并AMI患者PCI术后远期MACCEs的预测价值。方法纳入2014—2019年就诊于宁夏医科大学总医院心血管内科1683例T2DM合并AMI患者为研究对象,收集患者的一般临床资料与检查结果。对所有患者进行电话或门诊随访,以全因死亡、非致死性心肌梗死、再发不稳定型心绞痛、非致死性脑卒中、新发心力衰竭或心力衰竭加重再入院、再次血运重建作为MACCEs。根据患者随访期间是否发生MACCEs分为MACCEs组(508例)和非MACCEs组(1175例)。采用单因素及多因素Logistic回归分析探讨T2DM合并AMI患者MACCEs事件的影响因素。采用Kaplan-Meier法绘制患者的生存曲线,生存曲线的比较采用Log-rank检验。采用受试者工作特征(ROC)曲线分析CAR对T2DM合并AMI患者远期发生MACCEs的预测效能,使用净重分类改善指标(NRI)和综合判别指数(IDI)评价CAR对T2DM合并AMI患者预后评估的改善效果。结果1683例患者中508例(30.18%)患者发生MACCEs。多因素Logistic回归分析显示高血压病[OR(95%CI)=1.994(1.142~3.483)]、冠状动脉植入支架长度[OR(95%CI)=1.031(1.002~1.062)]、CRP[OR(95%CI)=0.950(0.915~0.986)]、Alb[OR(95%CI)=0.933(0.880~0.989)]及CAR[OR(95%CI)=5.582(1.705~18.277)]是T2DM合并AMI患者PCI术后发生MACCEs的影响因素(P<0.05)。根据CAR中位表达水平(0.86),将患者分为CAR<0.86组和CAR≥0.86组,Log-rank检验结果显示,CAR≥0.86组MACCEs发生率高于CAR<0.86组(52.68%与22.92%;χ^(2)=65.65,P<0.001)。ROC曲线显示CAR预测T2DM合并AMI患者发生MACCEs的ROC曲线下面积为0.728(95%CI=0.702~0.754),最佳截断值为0.576,灵敏度为0.617,特异度为0.747。在基线模型基础上,与CRP、Alb相比,CAR能明显改善对患者发生MACCEs的预测效果(NRI=0.377,IDI=0.166,C指数=0.690;P<0.05)。结论CAR是T2DM合并AMI患者PCI术后远期MACCEs发生风险的有效预测指标。

Protein C deficiency with venous and arterial thromboembolic events

Protein C(PC)is a key component of the vitamin K-dependent coagulation pathway.It exerts anticoagulant effects by inactivating factors V and VIII.Acquired or inherited PC deficiency results in a prothrombotic state,with presentations varying from asymptomatic to venous thromboembolism.However,there has been an increasing number of reports linking PC deficiency to arterial thromboembolic events,such as myocardial infarction and ischemic stroke.This editorial focuses on the association between PC deficiency and thromboembolism,which may provide some insights for treatment strategy and scientific research.

Activated Protein C Resistance in Patients with Pre-Eclampsia in Lagos, Nigeria

Background: Preeclampsia is reported to complicate 2% - 8% of pregnancies globally and is an important cause of maternal and perinatal morbidity and mortality. The aetiology and pathogenesis are still poorly understood and substantial improvement has not been made in the prediction, prevention and treatment of the disease. Objective: To compare the frequency of activated protein C resistance (APC-R) in patients with pre-eclampsia to that of normotensive pregnant women and to determine the correlation between activated protein ratio (APC-ratio) and the severity of pre-eclampsia. Methodology: A cross-sectional study was carried out in 100 pre-eclamptic patients and 100 normotensive pregnant controls. The APC-ratio was determined using the modified activated partial thromboplastin time. Study participants with APC-ratio of less than 2.0 were defined as having APC-R. Data was analyzed using SPSS version 22.0. Results: Mean APC-ratio was significantly lower in pre-eclamptics (2.89 ± 1.70) compared to normotensive pregnant women (3.57 ± 1.06) (p = 0.0008) and the levels were also higher in mild (2.95 ± 1.15) compared to severe pre-eclamptics (2.62 ± 1.14). The frequency of APC-R was 26% among women with pre-eclampsia compared to 4% among normotensive controls (p = 0.000). Among 100 pre-eclamptic women 7 (21.2%) out of 33 with mild pre–eclampsia had APC-R, while 19 (28.4%) out of 67 with severe pre-eclampsia had APC-R. APC-ratio had a significant negative correlation with mean arterial blood pressure (r = −0.324;p = 0.000) and proteinuria (r = −0.379;p = 0.000) among study participants. Conclusion: The frequency of activated protein c resistance is significantly higher in pre-eclamptics compared to normotensive pregnant women and this is more pronounced in those with severe pre-eclampsia compared with those with mild disease. APC-R may therefore be used as a marker of severity in the disease.

Endoplasmic reticulum stress and autophagy in cerebral ischemia/reperfusion injury:PERK as a potential target for intervention

Several studies have shown that activation of unfolded protein response and endoplasmic reticulum(ER)stress plays a crucial role in severe cerebral ischemia/reperfusion injury.Autophagy occurs within hours after cerebral ischemia,but the relationship between ER stress and autophagy remains unclear.In this study,we established experimental models using oxygen-glucose deprivation/reoxygenation in PC12 cells and primary neurons to simulate cerebral ischemia/reperfusion injury.We found that prolongation of oxygen-glucose deprivation activated the ER stress pathway protein kinase-like endoplasmic reticulum kinase(PERK)/eukaryotic translation initiation factor 2 subunit alpha(e IF2α)-activating transcription factor 4(ATF4)-C/EBP homologous protein(CHOP),increased neuronal apoptosis,and induced autophagy.Furthermore,inhibition of ER stress using inhibitors or by si RNA knockdown of the PERK gene significantly attenuated excessive autophagy and neuronal apoptosis,indicating an interaction between autophagy and ER stress and suggesting PERK as an essential target for regulating autophagy.Blocking autophagy with chloroquine exacerbated ER stress-induced apoptosis,indicating that normal levels of autophagy play a protective role in neuronal injury following cerebral ischemia/reperfusion injury.Findings from this study indicate that cerebral ischemia/reperfusion injury can trigger neuronal ER stress and promote autophagy,and suggest that PERK is a possible target for inhibiting excessive autophagy in cerebral ischemia/reperfusion injury.

Effect of Ultraviolet Radiation on Hsp70 Protein Expression in HaCaT Cells

Ultraviolet radiation by its wavelength is divided into: UVA, UVB and UVC. Only UVA and UVB manage to penetrate the ozone layer, but due to anthropological activities, all of them are capable of interacting with humans to a greater or lesser extent, and can generate adverse effects such as cellular stress when interacting with intra-and extracellular biomolecules. The skin is the first organ in contact with UV radiation, and the stress it generates can be analyzed by the expression of a bioindicator of cellular damage such as Hsp70. Therefore, the objective of the project was: to determine the effect of UVA, UVB and UVC radiation on HaCaT epithelial cells, by analyzing the expression of Hsp70. Materials and methods: HaCaT cells were cultured in vitro, which were irradiated with UVA, UVB and UVC light at different doses, to subsequently determine the degree of Hsp70 expression by Immunodetection by PAGE-SDS and Western Blot. Results: Basal expression of Hsp70 was observed in no irradiated HaCaT cells. When HaCaT cells were irradiated with UVA, UVB, UVC, an increase in this Hsp70 protein was observed. With UVA, a higher degree of expression was observed at a time of 30 minutes of irradiation. With UVB the highest expression shifted to a time of 20 minutes. With UVC, overexpression was observed after 10 minutes. Conclusion: UV radiation generates cellular stress on HaCaT cells, evaluated by the stress bioindicator Hsp70. According to the wavelength of UV radiation, those that have a shorter wavelength have a greater potential for cellular damage, such as UVC.

Bioinformatic identification of genes encoding C1q-domain-containing proteins in zebrafish

C1q is the first subcomponent of classical pathway in the complement system and a major link between innate and acquired immunities. The globular （gC1q） domain similar with C1q was also found in many non-complement C1q-domain-containing （C1qDC） proteins which have similar crystal structure to that of the multifunctional tumor necrosis factor （TNF） ligand family, and also have diverse functions. In this study, we identified a total of 52 independent gene sequences encoding C1q-domain-containing proteins through comprehensive searches of zebrafish genome, cDNA and EST databases. In comparison to 31 orthologous genes in human and different numbers in other species, a significant selective pressure was suggested during vertebrate evolution. Domain organization of C1q-domain-containing （C1qDC） proteins mainly includes a leading signal peptide, a collagen-like region of variable length, and a C-terminal C1q domain. There are 11 highly conserved residues within the C1q domain, among which 2 are invariant within the zebrafish gene set. A more extensive database searches also revealed homologous C1qDC proteins in other vertebrates, invertebrates and even bacterium, but no homologous sequences for encoding C1qDC proteins were found in many species that have a more recent evolutionary history with zebrafish. Therefore, further studies on C1q-domain-containing genes among different species will help us understand evolutionary mechanism of innate and acquired immunities.

Structure-activity Relationship of Phenothiazines for Inhibition of Protein Kinase C and Reversal of Multidrug Resistance

Studies on structure-activity relationship of phenothiazines (PTZs) forinhibition of protein kinase C (PKC) and reversal of multidrug resistance (MDR) has been made invitro. The results showed that the order of potency of reversal effect of PTZs on MDR is as follows:2-COC_3 H_7 > 2-CF_3 > 2-COCH_3 > H. The type of piperazinyl substitution also significantlyaffected potency against MDR. The results show the order: CH_3 > COOC_2 H_5 > C_2 H_4 OH. Inaddition, PKC plays a marked role in diverse cellular process including MDR. Some derivatives of PTZwas tested for inhibition of PKC, of which PTZ11 showed the highest inhibitory effect of MDR andPKC, implying a potential reversal agent of MDR for tumor therapy in the future. We also tried toexplore the possible binding model of PTZs to PKC. Our molecular-modeling study preliminarilysuggests how these PTZs bind to PKC and provides a structural basis for the design of high affinityPKC-modulator. The infor-mation may be used in the rational design of more effective drugs.

Correlation between C-reactive Protein and Morphology of Aortic Intramural Hematoma on CT Angiography

Objectives To investigate the morphologic characteristics of intramural hematoma(IMH)on CT angiography(CTA),and evaluate the possible correlation of serum C-reactive protein(CRP)with morphologic characteristics of IMH.Material and Methods Forty-two patients who were initially diagnosed as IMH by aortic CTA and also had serum CRP examination on the same day of CTA were enrolled in this retrospective study,including 30 males and 12 females,with the mean age of 61±14 years old.The volumetric CT data were retrospectively processed and analyzed on post-processing workstation.Based on the thickness of IMH and the length-area curve,the crosssectional area of true lumen and total vessel were measured,the hematoma-vessel ratio(HVR)was calculated.Imaging characteristics were compared between patients who had pathological elevated CRP(>0.8 mg/dl)and those did not.Spearman correlation analyses of CRP level and morphological characteristics of IMH were performed,and the receiver operating characteristic(ROC)curve was used to evaluate the diagnostic validity of CRP.Results Of all 42 IMH patients,the mean serum CRP was 3.94±4.71 mg/dl,and the mean HVR was 46.7%±14.2%.HVR in patients with elevated CRP was significantly higher than those with normal CRP(49.7%±15.0%vs.40.7%±10.5%,P=0.030).HVR was mildly correlated with CRP in all patients(r=0.48,P<0.001).CRP levels differed neither between patients with Stanford type A and B(P=0.207),nor between patients with and without intimal disruption(P=0.230).To discriminate HVR>47%(the mean value),the area under curve(AUC)were 0.700(95%CI:0.535-0.865)for CRP at a cutoff point of 3.55 mg/dl,with a sensitivity of 54.5%and a specificity of 90.0%.Conclusion CRP was mildly correlated with the severity of cross-sectional hematoma area of IMH,but not with Stanford types and the presence of intimal disruption.

血清PCT、CRP及IL-4水平预测小儿支原体肺炎病情严重程度的价值

目的:探讨血清降钙素原(PCT)、C反应蛋白(CRP)及白细胞介素-4(IL-4)水平预测支原体肺炎患儿病情严重程度的价值。方法:选取2019年1月—2023年1月淮安市第二人民医院儿科收治的102例支原体肺炎患儿作为研究对象,根据病情将患儿分为轻症组59例和重症组43例。比较两组临床资料及基质细胞衍生因子(CXCL12)、γ干扰素(IFN-γ)、硫化氢(H_(2)S)、超氧化物歧化酶(SOD)、基质金属蛋白酶-9(MMP-9)、PCT、CRP及IL-4水平,多因素分析采取非条件logistic逐步回归分析,采用ROC曲线分析PCT、CRP及IL-4水平对重症支原体肺炎的预测价值。结果:两组性别、年龄、病程及CXCL12、IFN-γ、H_(2)S、SOD、MMP-9水平比较,差异无统计学意义(P>0.05);重症组PCT、CRP、IL-4水平显著高于轻症组,差异有统计学意义(P<0.05)。logistic逐步回归分析结果显示,PCT、CRP及IL-4为重症支原体肺炎独立危险因素(P<0.05)。ROC分析显示,PCT、CRP及IL-4预测重症支原体肺炎的曲线下面积分别为0.896、0.851、0.787。结论:血清PCT、CRP及IL-4水平均参与支气管肺炎患儿的病情进展,且可作为重症支气管肺炎的诊断指标。

急性颅脑损伤患者CT评分变化及血清乳酸、NSE、CRP的相关性分析

目的探讨急性颅脑损伤(ACI)患者计算机断层扫描(CT)评分变化与血清乳酸(LA)、神经元特异性烯醇化酶(NSE)及C-反应蛋白(CRP)水平的关系及其对预后的预测价值。方法选取2020年1月—2022年1月东台市人民医院收治的50例急性颅脑损伤患者作为疾病组,根据患者治疗后格拉斯哥预后评分(GOS)分为预后良好组(32例)和预后不良组(18例);选取50例行健康体检受试者作为健康组。受试者工作特征曲线(ROC)评估血清乳酸、NSE、CRP水平与CT评分对急性颅脑损伤患者预后的评估价值。结果疾病组血清乳酸、NSE、CRP水平均高于健康组(P<0.05);预后不良组乳酸、NSE、CRP水平和CT评分均高于预后良好组;经Spearman相关分析,急性颅内损伤患者血清中乳酸、NSE、CRP水平与CT评分呈正相关(r=0.431、r=0.345、r=0.226,均P<0.05);ROC曲线分析显示,血清乳酸、NSE、CRP水平、CT评分联合预测急性颅内感染预后的曲线下面积(AUC)高于单一指标检测(P<0.05)。结论急性颅脑损伤患者CT评分与患者入院血清乳酸、NSE、CRP水平呈正相关,联合诊断对患者预后评估有一定价值。

血清超敏C反应蛋白、胱抑素C与脓毒性休克患者心功能、肾功能损伤的关系

目的检测脓毒性休克患者血清超敏C反应蛋白(hs-CRP)、胱抑素C(Cys C)水平,探讨其与脓毒性休克患者心功能、肾功能损伤的关系。方法选取2020年5月—2023年12月我院收治的脓毒性休克患者50例,纳入休克组。另选取同期健康体检者48名,纳入参照组。比较2组研究对象hs-CRP、Cys C水平,分析脓毒性休克患者血清hs-CRP、Cys C水平与患者左室射血分数(LVEF)、二尖瓣舒张早期血流峰速(E)/二尖瓣环舒张早期速度(E’)、血浆脑钠肽(BNP)、心肌肌钙蛋白Ⅰ(c TnⅠ)、肾小球滤过率(GFR)及急性生理学与慢性健康状况评分系统Ⅱ(APACHEⅡ)评分的关系。结果2组研究对象年龄、性别分布、身体质量指数(BMI)及基础疾病患病情况等方面的差异均无统计学意义(P>0.05)。休克组患者的血清hs-CRP水平[(181.01±37.39)mg/L]和血清Cys C水平[(2.62±0.25)mg/L]显著高于参照组[(38.78±10.55)mg/L、(0.96±0.15)mg/L],差异均有统计学意义(P<0.05)。休克组患者的血清hs-CRP水平与LVEF、E/E’、BNP、c TnⅠ水平、APACHEⅡ评分有关(P<0.05),与GFR无相关性(P>0.05);休克组患者的血清Cys C水平与GFR水平、APACHEⅡ评分有关(P<0.05),与LVEF、E/E’、BNP及c TnⅠ水平均无相关性(P>0.05)。结论脓毒性休克患者血清hs-CRP、Cys C水平均显著高于健康体验者,推测其可能与心肌细胞受损、炎症因子水平升高、肾血流量降低等因素有关,可作为评估脓毒性休克患者心、肾功能损伤的参考指标。

Lp-PLA2、hs-CRP和FIB联合检测在急性脑梗死诊断中的应用

目的探讨血浆脂蛋白相关磷脂酶A2(Lp-PLA2)、超敏C反应蛋白(hs-CRP)和纤维蛋白原(FIB)联合检测在急性脑梗死诊断中的临床价值。方法收集我院240例急性脑梗死的住院患者作为研究对象(脑梗组),以100例门诊体检健康人员为对照组,比较两组人群的一般临床数据及检验结果,记录患者入院时的NIHSS评分。分析急性脑梗死患者血浆Lp-PLA2、hs-CRP和FIB水平与其神经功能缺损程度的关系,进行多因素Logistic回归分析确定急性脑梗死的危险因素,利用ROC曲线评估患者血浆Lp-PLA2、hs-CRP和FIB水平对急性脑梗死的诊断价值。结果重度脑梗死患者的Lp-PLA2、hs-CRP和FIB水平均高于轻度及中度脑梗死患者(P<0.05);与对照组比较,脑梗组患者的血浆Lp-PLA2、hs-CRP和FIB水平均显著升高,差异均具有统计学意义(P<0.05)。血浆Lp-PLA2、hs-CRP和FIB水平与急性脑梗死发病风险显著相关(P<0.05)。Lp-PLA2、hs-CRP和FIB 3个指标中,Lp-PLA2的ROC曲线下面积最大,诊断价值最高;Lp-PLA2、hs-CRP和FIB联合检测能显著提高急性脑梗死的诊断效率。结论联合检测Lp-PLA2、hs-CRP和FIB对判断ACI患者神经功能缺损程度具有较高价值。

通督调神针法治疗阴虚动风型脑梗死偏瘫疗效及对患者血清Hcy、CRP水平的影响

目的:探讨通督调神针法治疗阴虚动风型脑梗死偏瘫患者疗效及对患者血清同型半胱氨酸(Hcy)、C反应蛋白(CRP)水平的影响。方法:选取脑梗死偏瘫患者76例,1∶1随机分为观察组(西医治疗+通督调神针法)与对照组(常规西医治疗)各38例。持续治疗1个月后,评估两组临床疗效,比较两组治疗前后中医证候积分、血清炎症因子(Hcy、CRP)水平、运动功能[Fugl-Meyer评定量表(FMA)]、平衡功能[Berg平衡量表(BBS)]和移动功能[功能性步态评价表(FGA)]变化情况,并记录两组不良事件发生率。结果:观察组总有效率更高(P<0.05);观察组治疗后中医证候积分降低程度比对照组更明显(P<0.05)。观察组治疗后FMA、FGA和BBS评分升高水平均比对照组更明显(P<0.05),观察组治疗后Hcy、CRP水平下降程度均比对照组更明显(P<0.05)。治疗期间两组均无不良事件发生。结论:阴虚动风型脑梗死偏瘫患者应用通督调神针法联合常规西医治疗具有较好的增益效果,可有效提高临床疗效,缓解患者临床症状,提高运动、平衡和移动能力,降低炎症反应。

脓毒症患者白细胞计数、血清C反应蛋白、肝素结合蛋白、降钙素原表达及与病情进展及预后关系

目的探讨白细胞计数(WBC)、血清C反应蛋白(CRP)、肝素结合蛋白(HBP)和降钙素原在脓毒症患者病情进展和预后评估中的应用价值。方法将2018年4月至2023年3月内江市第一人民医院收治的205例脓毒症患者纳入本次回顾性研究,根据病情严重程度分为脓毒症组(n=129)和脓毒性休克组(n=76),并根据患者预后情况分成存活组(n=154)和死亡组(n=51)。检测脓毒症组与脓毒性休克组、存活组与死亡组患者的WBC、血清CRP、HBP、降钙素原水平,收集患者的急性生理与慢性健康状况评分系统Ⅱ(APACHEⅡ)评分和序贯器官衰竭评估(SOFA)评分,分析WBC、血清CRP、HBP、降钙素原与APACHEⅡ、SOFA评分的相关性;采用受试者工作特征(ROC)曲线分析上述4个指标单独及联合检测评估脓毒症患者预后。结果脓毒性休克组的WBC、血清CRP、HBP、降钙素原分别为(19.83±3.09)×10^(9)/L、(114.10±35.17)mg/L、(78.92±13.14)μg/L和(11.13±0.91)μg/L,均显著高于脓毒症组[(9.55±2.87)×10^(9)/L、(59.96±23.45)mg/L、(36.47±12.83)μg/L和(8.21±0.82)μg/L],差异均有统计学意义(P<0.05)。脓毒性休克组的APACHEⅡ评分、SOFA评分分别为(20.05±2.39)、(10.29±2.51)分,均显著高于脓毒症组[(16.21±2.30)、(7.90±2.17)分],差异均有统计学意义(P<0.05)。Pearson相关性分析显示,WBC、血清CRP、HBP、降钙素原与APACHEⅡ评分(r=0.554、0.593、0.713、0.651,P<0.05)、SOFA评分均呈显著正相关(r=0.540、0.571、0.687、0.609,P<0.05)。死亡组的WBC、血清CRP、HBP、降钙素原、APACHEⅡ评分、SOFA评分也均显著高于存活组,差异均有统计学意义(P<0.05)。ROC曲线分析显示,WBC、血清CRP、HBP、降钙素原及4个指标联合检测预测脓毒症患者不良预后的ROC曲线下面积分别为0.835、0.803、0.881、0.817和0.939。结论脓毒性休克患者的WBC、血清CRP、HBP、降钙素原显著高于脓毒症患者,可反映脓毒症患者的病情严重程度,4个指标联合检测对脓毒症患者的预后有较好的预测价值。

D-二聚体与C反应蛋白对Stanford A型主动脉夹层动脉瘤患者术后远期预后的预测价值

目的分析D-二聚体(D-D)与C反应蛋白(CRP)在Stanford A型主动脉夹层动脉瘤(ADA)患者术后远期预后中的预测价值。方法选取76例胸痛患者为研究对象,所有患者均行心脏超声或主动脉CT血管成像检查,将45例Stanford A型ADA患者纳入观察组,均行手术治疗;非Stanford A型ADA的31例患者纳入对照组。对比2组发生胸痛72 h内的D-D与CRP水平。术后对观察组随访3年,按临床结局分成死亡组(n=10)与存活组(n=35),对比2组D-D与CRP水平;另绘制受试者工作曲线(ROC),分析D-D、CRP单独与联合预测Stanford A型ADA患者的远期预后临床价值。结果观察组的D-D[(1.31±0.35)mg/L]与CRP[(16.59±2.34)mg/L]水平高于对照组[(0.68±0.13)mg/L、(7.53±1.26)mg/L],差异有统计学意义(P<0.05);ADA患者中死亡组的D-D[(1.78±0.49)mg/L]与CRP[(30.46±4.77)mg/L]水平高于存活组[(1.03±0.26)mg/L、(13.59±2.36)mg/L],差异有统计学意义(P<0.05)。ROC结果显示,D-D与CRP联合检测预测Stanford A型ADA患者远期预后的曲线下面积(AUC)[0.909(95%CI:0.823~0.994)]高于D-D与CRP单独预测[0.806(95%CI:0.680~0.931)、0.840(95%CI:0.727~0.953)]。结论Stanford A型ADA患者血清内的D-D与CRP水平呈高表达,且表达水平越高,患者预后越差,两项指标联合可有效预测患者的远期预后,临床应用价值较高。