胸部肿瘤科护理交接班思维导图的制作及应用

目的探讨思维导图在胸部肿瘤科护理交接班中的应用效果。方法将胸部肿瘤Ⅰ病区16名护士设为观察组,Ⅱ病区16名护士设为对照组。对照组采用传统的交接班方法,观察组在传统交接班方法的基础上制作护理交接班思维导图,应用其进行系统交班。结果观察组住院患者和接班护士对交接班的满意度显著高于对照组(均P0.01),观察组交班缺陷发生率显著低于对照组(P0.05,P0.01)。结论专科护理交接班思维导图的制作具有针对性,将其用于胸部肿瘤科交接班有利于提高住院患者和接班护士的满意度,提高交接班质量。     

心力衰竭患者家庭运动行为的自我效能干预

目的探讨运动自我效能干预对心力衰竭患者家庭运动行为的影响。方法将2016年5~7月住院符合纳入标准的40例患者作为对照组,8~10月38例患者作为干预组。对照组进行常规健康教育,干预组针对患者运动自我效能进行干预。分别评估患者入组时和出院后4个月的运动自我效能,并嘱患者出院后记录运动日志(包括运动形式、频率、时间和强度等)。对完成随访且资料完整的71例患者(对照组37例,干预组34例)的数据进行分析。结果干预后,干预组运动自我效能得分和运动频率、时间及强度显著优于对照组(P0.05,P0.01)。结论运动自我效能干预能有效提高心力衰竭患者的运动自我效能水平,改善家庭运动行为。     

ICU医护合作与护士职业获益感的相关性研究

目的调查ICU医护合作关系及ICU护士职业获益感,分析医护合作对护士职业获益感的影响。方法采用医护合作量表、护士职业获益感量表对230名ICU护士进行调查。结果医护合作量表总分为(90.60±14.48)分,条目均分为(3.62±0.58)分;护士职业获益感总分为(133.39±17.11)分,条目均分为(4.04±0.52)分。回归分析显示,护士和医生的关系、患者信息的交流能力及职称是护士职业获益感的主要影响因素(调整R2=0.428)。结论ICU医护合作和护士职业获益感较高,且医护合作是护士职业获益感的重要影响因素,管理者应重视医护合作关系的建设,提升护士的积极职业认知。     

腹腔镜胰体尾切除术28例分析

目的探讨腹腔镜胰体尾切除术(laparoscopic distal pancreatectomy,LDP)的可行性及临床价值。方法回顾分析2014年5月至2016年9月28例施行LDP病人的临床资料。28例病人中,男性9例,女性19例,年龄17~69岁。结果 16例LDP联合脾脏切除,7例行Kimura法保脾LDP,5例行Warshaw法保脾LDP。术后病理:胰腺浆液性囊腺瘤2例,黏液性囊腺瘤9例,实性假乳头状瘤6例,导管内乳头状黏液性肿瘤(intraductal papillary mucinous neoplasm,IPMN)3例,胰岛素瘤3例,胰腺假性囊肿1例,慢性胰腺炎1例,胰腺癌3例。全组病人平均手术时间为(203±54)min;平均术中出血量为(115±138)ml。平均术后下床活动时间为(1.4±0.6)d;平均术后首次进食时间为(2.0±0.8)d;平均术后住院时间为(10±5)d。术后发生胰瘘9例(32.1%),其中A级胰瘘6例,未予特殊处理,自然痊愈;B级胰瘘3例,均经冲洗引流后痊愈。术后发生脾部分梗死2例,未予特殊处理,经3个月随访观察自然痊愈。结论 LDP安全可行,具有微创优势,值得推广应用。     

腹腔镜联合胆道镜治疗复发胆管结石的临床体会

目的探讨腹腔镜联合胆道镜治疗复发胆管结石的临床可行性与安全性。方法回顾性分析2013年1月至2015年1月华中科技大学同济医学院附属荆州医院收治的90例因复发胆管结石施行腹腔镜下胆总管探查、胆道镜取石病人的临床资料。结果 90例病人中86例成功施行腹腔镜手术,其中4例中转开腹。手术时间为(123.0±34.6)min,术中胆道取石时间为(64.0±12.4)min,术中出血量为(31.4±13.5)ml,术后平均住院时间为(6.8±2.5)d。围手术期主要并发症是胆漏。所有病人随访期内无结石复发,无胆管狭窄发生。结论腹腔镜联合胆道镜治疗复发胆管结石是安全有效的,应作为复发胆管结石再手术的首选手术方式。     

胃癌合并胆囊疾病同期切除的可行性与安全性研究

目的 探讨合并胆囊疾病的胃癌患者同期行胃癌根治术及胆囊切除术的可行性及安全性。方法 1996-01—2011-01间中国人民解放军第二五四医院共手术治疗800例胃癌患者。将722例未合并胆囊疾病患者作为对照组,行根治性胃癌切除术。将78例合并有胆囊疾病的患者作为观察组,同期行根治性胃癌切除术和胆囊切除术。回顾性分析患者的临床资料。结果 观察组的手术时间长于对照组,差异有统计学意义(P0.05)。2组患者术中出血量、住院时间、术后并发症发生率,术后3 d引流量、下床时间、术后排气时间及5 a生存率比较,差异均无统计学意义(P0.05)。结论 对合并有胆囊疾病的胃癌患者同期行胃癌根治术及胆囊切除术,安全可行。     

Cartilage‐Specific Autophagy Deficiency Promotes ER Stress and Impairs Chondrogenesis in PERK‐ATF4‐CHOP–Dependent Manner

Autophagy is activated during nutritionally depleted or hypoxic conditions to facilitate cell survival. Because growth plate is an avascular and hypoxic tissue, autophagy may have a crucial role during chondrogenesis; however, the functional role and underlying mechanism of autophagy in regulation of growth plate remains elusive. In this study, we generated ^TamCartAtg7^–/– (Atg7cKO) mice to explore the role of autophagy during endochondral ossification. Atg7cKO mice exhibited growth retardation associated with reduced chondrocyte proliferation and differentiation, and increased chondrocyte apoptosis. Meanwhile, we observed that Atg7 ablation mainly induced the PERK‐ATF4‐CHOP axis of the endoplasmic reticulum (ER) stress response in growth plate chondrocytes. Although Atg7 ablation induced ER stress in growth plate chondrocytes, the addition of phenylbutyric acid (PBA), a chemical chaperone known to attenuate ER stress, partly neutralized such effects of Atg7 ablation on longitudinal bone growth, indicating the causative interaction between autophagy and ER stress in growth plate. Consistent with these findings in vivo, we also observed that Atg7 ablation in cultured chondrocytes resulted in defective autophagy, elevated ER stress, decreased chondrocytes proliferation, impaired expression of col10a1, MMP­13, and VEGFA for chondrocyte differentiation, and increased chondrocyte apoptosis, while such effects were partly nullified by reduction of ER stress with PBA. In addition, Atg7 ablation‐mediated impaired chondrocyte function (chondrocyte proliferation, differentiation, and apoptosis) was partly reversed in CHOP^–/– cells, indicating the causative role of the PERK‐ATF4‐CHOP axis of the ER stress response in the action of autophagy deficiency in chondrocytes. In conclusion, our findings indicate that autophagy deficiency may trigger ER stress in growth plate chondrocytes and contribute to growth retardation, thus implicating autophagy as an important regulator during chondrogenesis and providing new insights into the clinical potential of autophagy in cartilage homeostasis. © 2017 American Society for Bone and Mineral Research.     

Dysfunction of Caveolae-Mediated Endocytic TβRI Degradation Results in Hypersensitivity of TGF-β/Smad Signaling in Osteogenesis Imperfecta

Osteogenesis imperfecta (OI) is a genetic disorder caused by mutations of type I collagen-related genes, and excessive transforming growth factor-beta (TGF-β) signaling is a common mechanism. TGF-β/Smad signaling has inhibitory effects on osteoblast differentiation and maturation and is mainly transduced and regulated by the internalization of a tetrameric receptor complex comprising types I and II TGF-β receptors (TβRI and TβRII). During internalization, clathrin-mediated endocytosis enhances TGF-β/Smad signaling via Smad2/3 phosphorylation and receptors recycling, while caveolae-mediated endocytosis turns off TGF-β/Smad signaling by promoting receptor ubiquitination and degradation. In this study, using an animal model of OI (Colla2^oim, osteogenesis imperfecta murine [oim]/oim mouse), we found that osteoblastic cells of oim/oim mice were more sensitive to the inhibitory effects of TGF-β on osteoblast differentiation and maturation and had much higher cell membrane protein levels of TGF-β receptors than those of wild-type (wt)/wt mice. Further results showed that clathrin-mediated endocytosis of TβRI was enhanced, whereas caveolae-mediated TβRI endocytic degradation was reduced in oim/oim mice, combined with reduced caveolin-1 (Cav-1) phosphorylation. In addition, type I collagen downregulated TβRI via focal adhesion kinase (FAK) and Src activation-dependent Cav-1 phosphorylation. To further examine this mechanism, 4-week-old oim/oim and wt/wt mice were treated with either TβRI kinase inhibitor (SD-208) or vehicle for 8 weeks. SD-208 treatment significantly reduced the fracture incidence in oim/oim mice. Micro–computed tomography and biomechanical testing showed that femoral bone mass and strength were significantly improved with SD-208 treatment in both genotypes. Additionally, SD-208 significantly promoted osteoblast differentiation and bone formation and inhibited bone resorption. In conclusion, dysfunction of caveolae-mediated endocytic TβRI degradation is a possible mechanism for the enhanced TGF-β/Smad signaling in OI. Targeting this mechanism using a TβRI kinase inhibitor effectively reduced fractures and improved bone mass and strength in OI model and, thus, may offer a new strategy for the treatment of OI. © 2022 American Society for Bone and Mineral Research (ASBMR).     

C-reactive protein to albumin ratio (CAR) in predicting surgical site infection (SSI) following instrumented posterior lumbar interbody fusion (PLIF)

Identification of novel markers would contribute to the individualised risk assessment and development of a risk prediction model. This study aimed to investigate the role of the C-reactive protein to albumin ratio (CAR) in predicting surgical site infection (SSI) following instrumented posterior lumbar interbody fusion (PLIF) of lumbar degenerative diseases. This study enrolled patients who underwent PLIF and instrumentation for treatment of lumbar degenerative diseases between 2015 and 2020. Electronic medical records were inquired for data collection, with follow-up register for identifying SSI cases. The optimal cut-off for CAR was determined by constructing the receiver operator characteristic (ROC) curve. Patients with high- or low-CAR value were compared using the univariate analyses, and the association between CAR and the risk of SSI was investigated using multivariate logistics regression analysis. A total of 905 patients were enrolled, twenty-nine (3.2%) had developed an SSI with 72.4% occurring during index hospitalisation, and 11 (1.2%) had deep and 18 (2.0%) superficial SSIs. An SSI was associated with additional 10.7 days of index total hospital stay (P = .001). The CAR was 0–5.43 (median, 0.05), and the optimal cut-off was 0.09 and area under the curve was 0.720 (P < .001). 336 (37.1%) patients had a CAR ≥0.09 and 22 (6.5%) developed an SSI, with a crude risk of 5.6 relative to those with a low CAR. The multivariate analyses showed CAR ≥0.09 was associated with 8.06-fold increased risk of SSI, together with diabetes (P = .018), while hypertension was identified as a protective factor (OR, 0.34; 95%CI, 0.11–1.00, P = .049). High CAR is found to significantly predict the incident SSI following instrumented PLIF of lumbar degenerative diseases, and can be considered as a useful index in practice only after it is verified by future high-level evidences.