A Patient-Level Meta-Analysis of Intensive Glucose Control in Critically Ill Adults.

BACKGROUND: Whether intensive glucose control reduces mortality in critically ill patients remains uncertain. Patient-level meta-analyses can provide more precise estimates of treatment effects than are currently available. METHODS: We pooled individual patient data from randomized trials investigating intensive glucose control in critically ill adults. The primary outcome was in-hospital mortality. Secondary outcomes included survival to 90 days and time to live cessation of treatment with vasopressors or inotropes, mechanical ventilation, and newly commenced renal replacement. Severe hypoglycemia was a safety outcome. RESULTS: Of 38 eligible trials (n=29,537 participants), 20 (n=14,171 participants) provided individual patient data including in-hospital mortality status for 7059 and 7049 participants allocated to intensive and conventional glucose control, respectively. Of these 1930 (27.3%) and 1891 (26.8%) individuals assigned to intensive and conventional control, respectively, died (risk ratio, 1.02; 95% confidence interval [CI], 0.96 to 1.07; P=0.52; moderate certainty). There was no apparent heterogeneity of treatment effect on in-hospital mortality in any examined subgroups. Intensive glucose control increased the risk of severe hypoglycemia (risk ratio, 3.38; 95% CI, 2.99 to 3.83; P<0.0001). CONCLUSIONS: Intensive glucose control was not associated with reduced mortality risk but increased the risk of severe hypoglycemia. We did not identify a subgroup of patients in whom intensive glucose control was beneficial. (Funded by the Australian National Health and Medical Research Council and others; PROSPERO number CRD42021278869.).

Intensive glucose control in critically ill adults: a protocol for a systematic review and individual patient data meta-analysis / Controle intensivo da glicose em adultos em estado grave: um protocolo de revisão sistemática e metanálise de dados individuais de pacientes

ABSTRACT Objective: The optimal target for blood glucose concentration in critically ill patients is unclear. We will perform a systematic review and meta-analysis with aggregated and individual patient data from randomized controlled trials, comparing intensive glucose control with liberal glucose control in critically ill adults. Data sources: MEDLINE®, Embase, the Cochrane Central Register of Clinical Trials, and clinical trials registries (World Health Organization, clinical trials.gov). The authors of eligible trials will be invited to provide individual patient data. Published trial-level data from eligible trials that are not at high risk of bias will be included in an aggregated data meta-analysis if individual patient data are not available. Methods: Inclusion criteria: randomized controlled trials that recruited adult patients, targeting a blood glucose of ≤ 120mg/dL (≤ 6.6mmol/L) compared to a higher blood glucose concentration target using intravenous insulin in both groups. Excluded studies: those with an upper limit blood glucose target in the intervention group of > 120mg/dL (> 6.6mmol/L), or where intensive glucose control was only performed in the intraoperative period, and those where loss to follow-up exceeded 10% by hospital discharge. Primary endpoint: In-hospital mortality during index hospital admission. Secondary endpoints: mortality and survival at other timepoints, duration of invasive mechanical ventilation, vasoactive agents, and renal replacement therapy. A random effect Bayesian meta-analysis and hierarchical Bayesian models for individual patient data will be used. Discussion: This systematic review with aggregate and individual patient data will address the clinical question, 'what is the best blood glucose target for critically ill patients overall?' Protocol version 0.4 - 06/26/2023 PROSPERO registration: CRD42021278869

RESUMO Objetivo: Não está claro qual é a meta ideal de concentração de glicose no sangue em pacientes em estado grave. Realizaremos uma revisão sistemática e uma metanálise com dados agregados e de pacientes individuais de estudos controlados e randomizados, comparando o controle intensivo da glicose com o controle liberal da glicose em adultos em estado grave. Fontes de dados: MEDLINE®, Embase, Cochrane Central Register of Clinical Trials e registros de ensaios clínicos (Organização Mundial da Saúde, clinical trials.gov). Os autores dos estudos qualificados serão convidados a fornecer dados individuais de pacientes. Os dados publicados em nível de ensaio qualificado que não apresentem alto risco de viés serão incluídos em uma metanálise de dados agregados se os dados individuais de pacientes não estiverem disponíveis. Métodos: Critérios de inclusão: ensaios clínicos controlados e randomizados que recrutaram pacientes adultos, com meta de glicemia ≤ 120mg/dL (≤ 6,6mmol/L) comparada a uma meta de concentração de glicemia mais alta com insulina intravenosa em ambos os grupos. Estudos excluídos: aqueles com meta de glicemia no limite superior no grupo de intervenção > 120mg/dL (> 6,6mmol/L), ou em que o controle intensivo de glicose foi realizado apenas no período intraoperatório, e aqueles em que a perda de seguimento excedeu 10% até a alta hospitalar. Desfecho primário: Mortalidade intra-hospitalar durante a admissão hospitalar. Desfechos secundários: Mortalidade e sobrevida em outros momentos, duração da ventilação mecânica invasiva, agentes vasoativos e terapia de substituição renal. Utilizaremos metanálise bayesiana de efeito randômico e modelos bayesianos hierárquicos para dados individuais de pacientes. Discussão: Essa revisão sistemática com dados agregados e de pacientes individuais abordará a questão clínica: Qual é a melhor meta de glicose no sangue de pacientes graves em geral? Protocolo versão 0.4 - 26/06/2023 Registro PROSPERO: CRD42021278869

Physical therapy for end-stage hemophilic arthropathy: a case report.

This report introduces a young adult who has been in bed for more than ten years with end-stage hemophilic arthropathy. He didn't have access to factor VIII (FVIII) in the early stage of hemophilia due to the high costs of clotting replacement therapy. As a result, he is experiencing some difficulties, such as joint contracture, muscular atrophy, severe pain, and poor function of cardiopulmonary. He came to visit us for a comprehensive rehabilitation program, and, finally, he achieved the basic goal of self-care in daily life.

Daily point-of-care ultrasound-assessment of central venous catheter-related thrombosis in critically ill patients: a prospective multicenter study.

PURPOSE: Central venous catheter (CVC)-related thrombosis (CRT) is a known complication in critically ill patients. However, its clinical significance remains unclear. The objective of the study was to evaluate the occurrence and evolution of CRT from CVC insertion to removal. METHODS: A prospective multicenter study was conducted in 28 intensive care units (ICUs). Duplex ultrasound was performed daily from CVC insertion until at least 3 days after CVC removal or before patient discharge from the ICU to detect CRT and to follow its progression. CRT diameter and length were measured and diameter > 7 mm was considered extensive. RESULTS: The study included 1262 patients. The incidence of CRT was 16.9% (95% confidence interval 14.8-18.9%). CRT was most commonly found in the internal jugular vein. The median time from CVC insertion to CRT onset was 4 (2-7) days, and 12% of CRTs occurred on the first day and 82% within 7 days of CVC insertion. CRT diameters > 5 mm and > 7 mm were found in 48% and 30% of thromboses. Over a 7-day follow-up, CRT diameter remained stable when the CVC was in place, whereas it gradually decreased after CVC removal. The ICU length of stay was longer in patients with CRT than in those without CRT, and the mortality was not different. CONCLUSION: CRT is a frequent complication. It can occur as soon as the CVC is placed and mostly during the first week following catheterization. Half of the thromboses are small but one-third are extensive. They are often non-progressive and may be resolved after CVC removal.

Intensive glucose control in critically ill adults: a protocol for a systematic review and individual patient data meta-analysis.

OBJECTIVE: The optimal target for blood glucose concentration in critically ill patients is unclear. We will perform a systematic review and meta-analysis with aggregated and individual patient data from randomized controlled trials, comparing intensive glucose control with liberal glucose control in critically ill adults. DATA SOURCES: MEDLINE®, Embase, the Cochrane Central Register of Clinical Trials, and clinical trials registries (World Health Organization, clinical trials.gov). The authors of eligible trials will be invited to provide individual patient data. Published trial-level data from eligible trials that are not at high risk of bias will be included in an aggregated data meta-analysis if individual patient data are not available. METHODS: Inclusion criteria: randomized controlled trials that recruited adult patients, targeting a blood glucose of ≤ 120mg/dL (≤ 6.6mmol/L) compared to a higher blood glucose concentration target using intravenous insulin in both groups. Excluded studies: those with an upper limit blood glucose target in the intervention group of > 120mg/dL (> 6.6mmol/L), or where intensive glucose control was only performed in the intraoperative period, and those where loss to follow-up exceeded 10% by hospital discharge. PRIMARY ENDPOINT: In-hospital mortality during index hospital admission. Secondary endpoints: mortality and survival at other timepoints, duration of invasive mechanical ventilation, vasoactive agents, and renal replacement therapy. A random effect Bayesian meta-analysis and hierarchical Bayesian models for individual patient data will be used. DISCUSSION: This systematic review with aggregate and individual patient data will address the clinical question, 'what is the best blood glucose target for critically ill patients overall?'Protocol version 0.4 - 06/26/2023PROSPERO registration:CRD42021278869.

Blood circulation activating effect of Sanqi (Radix Notoginseng) on venous thromboembolism rat.

OBJECTIVE: To explore the blood circulation activating effect and mechanism of Sanqi (Radix Notoginseng) in vivo, using a venous thromboembolism (VTE) rat model. METHODS: We established the VTE rat model, and then intervened with low molecular weight heparin (LMWH), as well as low, medium and high doses of Sanqi (Radix Notoginseng), to observe the blood circulation activating effect of Sanqi (Radix Notoginseng) on VTE rats. RESULTS: After the treatment with high concentrations of Sanqi (Radix Notoginseng), the pulmonary thromboembolism was alleviated, and the lower limb thrombosis was markedly improved. Moreover, the expression quantities of plasma activated partial thromboplastin time, prothrombin time and D-dimer, as well as endothelin, von Willebrand factor, and plasminogen activator inhibitor-1 in thrombosis segment tissues were markedly down-regulated; while those of nitric oxide and tissue-type plasminogen activator were up-regulated. After low and medium concentration Sanqi (Radix Notoginseng) treatment, no obvious improvement was observed in each index. Moreover, the high concentration Sanqi (Radix Notoginseng) showed comparable efficacy to the positive drug LMWH. CONCLUSION: This data suggests that high concentration of Sanqi (Radix Notoginseng) is effective in preventing and treating VTE.

Efficacy of Sanqi (Radix Notoginseng) in treating cerebral hemorrhage in rats with traumatic brain injury.

OBJECTIVE: To evaluate the protective efficacy of Sanqi (Radix Notoginseng) on cerebral hemorrhage in a rat model of traumatic brain injury (TBI) by investigating plasminogen activator inhibitor-1 (PAI-1), tissue-type plasminogen activator (t-PA), nuclear factor-κB (NF-κB, p-p65), nitric oxide (NO), endothelin (ET), cluster differentiation (CD61CD62), and coagulation. METHODS: The free-fall method was used to create a rat model of TBI. Forty-eight rats were randomly divided into six groups: the blank group, sham group, model group, low-dose Sanqi (Radix Notoginseng) group, middle-dose Sanqi (Radix Notoginseng) group, and high-dose Sanqi (Radix Notoginseng) group. At 24 h after the model was created, we investigated brain MRI, brain tissue morphology using HE staining, flow cytometry, and immunohistochemical changes. RESULTS: Cerebral hemorrhage was aggravated in TBI rats (observed in brain specimens, brain MRI, and brain tissue HE). Cerebral immunohistochemistry results demonstrated that the expression of t-PA, PAI-1 and p-p65 increased significantly in TBI rats, while t-PA/PAI-1 had a significant decrease. In addition, CD61CD62, D2D, and ET were significantly increased in TBI rats, and PT and APTT were significantly prolonged; in contrast, NO was significantly decreased. Sanqi (Radix Notoginseng) decreased cerebral hemorrhage in TBI rats (observed in brain MRI and brain tissue HE), and increased t-PA/PAI-1, CD61CD62 significantly. It also significantly decreased the expression of t-PA, PAI-1, and p-p65 in brain immunohistochemistry and significantly decreased PT, APTT, D2D, and ET. However, there were no differences in NO between the model group and the Sanqi (Radix Notoginseng) group. CONCLUSION: Sanqi (Radix Notoginseng) can decrease the expression of p-p65, increase t-PA/PAI-1, and stem traumatic intracranial hemorrhage in a TBI rat model.

Panax notoginseng protects the rat brain function from traumatic brain injury by inhibiting autophagy via mammalian targeting of rapamycin.

Traumatic brain injury (TBI) remains one of the leading causes of death and disability worldwide. Our previous studies have found that traditional Chinese medicine, Panax notoginseng (P. notoginseng) can reduce cerebral hemorrhage in rats with TBI. Yet, the exact mechanism still remains unclear. According to the random number table, 36 SD rats were randomly divided into six groups: Sham group (negative control group), Model group, PIK inhibitor group (positive group), P. notoginseng group (experimental group), Rapamycin group, and Panax notoginseng+Rapamycin group (experimental group). In the Model group (M group, the group showing signs of TBI without any treatment), the neural function defect score was significantly decreased, while sequestosome 1 (P62), Beclin 1, and microtubule-associated protein 1 light chain 3 (LC3-II) were significantly increased. The brain tissue was significantly damaged, and many autophagosomes were observed in the cytoplasm. Compared with the Model group and the Rapamycin group (M+Rapa group, the group showing signs of TBI with Rapamycin treatment), P62, Beclin 1, and LC3-II were significantly decreased, the score of neural function defect was significantly improved, and the brain tissue damage was significantly reduced in the PIK (phosphatidylinositol 3-kinase) inhibitor group (M+LY group, the group showing signs of TBI with PIK inhibitor treatment). Compared with the Model group, mTOR was decreased and LC3-II was increased; however, there were no significant changes in neural function defect score, HE staining, Nissl staining, and transmission electron microscopy in the Rapamycin group. Compared with the Model group, the neural function defect score at 72h was significantly improved, mTOR was significantly increased, P62, Beclin 1, and LC3-II significantly decreased, brain tissue damage was reduced in HE staining and Nissl staining, autophagosomes were reduced in cytoplasm by transmission electron microscopy in the P. notoginseng group (M+PN group, the group showing signs of TBI with P. notoginseng treatment). Also, there was no significant difference between P. notoginseng group and P. notoginseng+Rapamycin group (M+PN+Rapa group, the group showing signs of TBI with P. notoginseng+Rapamycin treatment). P. notoginseng protects the rat brain function from TBI by inhibiting autophagy through the mTOR signaling pathway and other autophagy pathways.

Hsa_circ_103973 Acts as a Sponge of miR-335 to Promote Cervical Cancer Progression.

BACKGROUND: Cervical cancer (CC) ranks as the second most common malignancy in women, accounting for more two 2 million deaths every year in the world. Recently, circular RNAs (circRNAs) have been reported to regulate the progression of multiple human tumors; however, whether it involves in CC remains largely elusive. MATERIALS AND METHODS: Two GEO circRNA expression profiles (GSE102686, GSE113696) were downloaded to analyze the differentially expressed circRNAs using bioinformatics methods. Expression of circ_103973, miR-335 and PPP6C in CC tissues and cell lines were examined by qRT-PCR. Cell apoptosis was assessed with PI/Annexin-V double staining followed by the analysis of flow cytometry. Cell proliferation was evaluated by MTT and colony formation assays. Interaction between circ_103973 and miR-335, as well as miR-335 and PPP6C, were verified by dual-luciferase reporter assay. RESULTS: Circ_103973 was found to be highly expressed in both GSE102686 and GSE113696 datasets as well as in CC tissue samples and cell lines. Higher levels of circ_103973 were correlated to a worse outcome of CC patients. Knockdown of circ_103973 significantly promoted CC cell apoptosis and inhibited CC cell proliferation in vitro. Mechanistically, we demonstrated that circ_103973 served as a sponge of miR-335, which directly targeted PPP6C in CC cells. miR-335 was found to be decreased in CC, while PPP6C was found to be increased in CC. Moreover, anti-miR-335 could reverse the inhibitory effects of circ_103973 knockdown on CC cell proliferation, and this phenomenon could be blocked by si-PPP6C. CONCLUSION: Circ_103973 promoted CC cell proliferation in vitro by physically binding miR-335, which further targeted and regulated PPP6C.

Use of autologous platelet rich fibrin-based bioactive membrane in pressure ulcer healing in rats.

OBJECTIVE: To verify the feasibility of treating pressure ulcers (PUs) with autologous platelet-rich fibrin-based (PRF) bioactive membrane, both in vitro and in vivo. METHOD: An animal model using adult male Sprague-Dawley rats was used. Pressure was periodically exerted on the skin to induce localised ischaemia by using an external magnet and transplanted metal disc. After a PU developed, the rats were divided into two groups: a treatment group and a control group. Rats in the treatment group were then treated with PRF bioactive membrane every three days. RESULTS: A total of 20 rats were used in this study. At days three and seven, the PU area in the PRF bioactive membrane-treated group was significantly smaller than that in the control group, and after 14 days of treatment, the PUs in the PRF bioactive membrane treatment group had healed. Haemotoxylin and eosin staining, immunohistochemistry and Western blot results indicated that PRF bioactive membrane induced wound healing by increasing the thickness of the regenerated epidermis and by upregulating vascular endothelial growth factor expression. Further, we found that different concentrations of rat autologous PRF soluble factors extraction components could significantly promote rat aortic endothelial cell proliferation, wound healing and migration ability in vitro. CONCLUSION: Overall, results indicate that PRF bioactive membrane promotes PU healing in rats. Thus, it may represent a natural and effective wound-healing tool for use in the treatment of clinical skin PUs in humans in the future.

Effects of Ischemic Post-Conditioning on the Expressions of LC3-II and Beclin-1 in the Hippocampus of Rats After Cerebral Ischemia and Reperfusion.

OBJECTIVE: To investigate the effects of postconditioning ischemia on the expressions of the hippocampus neuron autophagy-related proteins LC3-II and Beclin-1 in rats following cerebral ischemia reperfusion. METHODS: A total of 128 male Sprague-Dawley rats were randomly divided into 4 groups: control, cerebral ischemia-reperfusion (IR), cerebral ischemia post-conditioning group (IP), and PI3K/Akt inhibitor (LY294002). The rat cerebral ischemia model was established by the improved Pulsinelli four vessel occlusion method. The durations across the platform and escape latent period were recorded using the water maze experiment. The changes in cell morphology and the number of surviving hippocampal neurons were detected by hematoxylin-eosin (HE) staining. The cells with Beclin-1 and LC3-II in the hippocampal region were detected by immunohistochemical staining and Western blotting. RESULTS: When compared with the IR at 48 and 72 h, the number of platform passes increased and the escape latency time was shortened. Consequently, the HE staining detected positive cells with LC3-II and Beclin-1 increased in number at each time point in immunohistochemistry and the expressions of the LC3-II and Beclin-1 proteins were improved in the IP (P < 0.05). CONCLUSIONS: Cerebral ischemic post-conditioning promoted the expressions of autophagy-related proteins LC3-II and Beclin-1 while relieving the injuries caused by cerebral ischemia reperfusion.

Effect of electroacupuncture at ST36 on the intestinal mucosal mechanical barrier and expression of occludin in a rat model of sepsis.

OBJECTIVE: To observe the effect of electroacupuncture (EA) at ST36 on the intestinal mucosal mechanical barrier and expression of the tight junction (TJ) protein, occludin, in a rat model of sepsis. METHODS: 60 male Wistar rats were randomly divided into six groups (n=10 rats each): Control, Control+EA, CLP (caecal ligation and puncture), CLP+EA, CLP+Sham-EA, and Sham-CLP. Rats of the CLP, CLP+EA and CLP+Sham-EA groups underwent CLP modeling of sepsis; those in the Sham-CLP underwent sham surgery and those in the Control and Control+EA groups remained unoperated. Rats in the CLP+EA and Control+EA groups received verum EA at ST36 and rats in the CLP+Sham-EA groups received EA at non-traditional acupuncture points. After three days, serum D-lactate concentrations were measured and ileal mucosa was collected for haematoxylin and eosin staining, morphological observation and Chiu's scoring. The intestinal epithelial cells were observed under transmission electron microscopy (TEM), while protein expression of occludin was measured by immunohistochemistry and Western blotting. RESULTS: TJs of the Control, Sham-CLP and Control+EA groups were continuous under TEM but discontinuous in the CLP, CLP+EA and CLP+Sham-EA groups. Plasma D-lactate levels were significantly higher in the CLP, CLP+EA and CLP+Sham-EA groups compared with the Control, Sham-CLP and Control+EA groups (P<0.01). Protein expression of occludin, reflected by immunohistochemistry scores (IHS) and the results of Western blotting, were significantly reduced in the CLP, CLP+EA and CLP+Sham-EA groups when compared with the Control, Sham-CLP and Control+EA groups (P<0.01). Compared with the CLP group, the IHS and Western blotting results of the CLP+EA group were both significantly higher (P<0.05), while those of the CLP+Sham-EA group were similar to the CLP group. CONCLUSIONS: Electrical stimulation at ST36 in rats with sepsis can increase protein expression of occludin, reduce serum D-lactate levels and increase permeability of the intestinal barrier.

Hot Compress with Chinese Herbal Salt Packets Reducing PICC Catheter Complications: A Randomized Controlled Trial.

OBJECTIVE: To explore the preventive effect of applying hot compress with Chinese herbal salt packets (CHSP) to puncture vessels under aseptic conditions during peripherally inserted central catheter (PICC) on postoperative phlebitis. METHODS: A total of 720 hospitalized patients undergoing first PICC were assigned to treatment and control groups (360 cases each group) according to a random number table. The control group received conventional catheterization and nursing care. The treatment group was first given hot compress with CHSP (which consisted of honeysuckle 30 g, Semen brassicae 30 g, Salvia miltiorrhiza 30 g, Angelica dahurica 30 g, Semen raphani 30 g, Evodia rutaecarpa 30 g, and coarse salt 20 g) on the punctured vessel under aseptic conditions for 5-10 min before conventional catheterization. The main efficacy indices were the vessel diameters before and during catheterization and the success rate of a single catheter, and the secondary efficacy indiex was the incidence of superficial phlebitis within 1 week after catheterization. RESULTS: The vessel diameter during catheterization of the treatment group was remarkably increased compared with the control group [(7.96±0.42) mm vs. (4.39±0.54) mm, P<0.01]. The success rate of the single catheter of the treatment group was significantly higher than that of the control group [94.00% (329/350) vs. 73.72% (244/329), P<0.01]. The incidence of superficial phlebitis within 1 week after catheterization in the treatment group was lower than that in the control group (P=0.007). There was no adverse event with CHSP. CONCLUSION: Hot compress with CHSP during PICC is applicable as it can effectively improve the success rate of a single catheter and reduce the incidence of superficial phlebitis after catheterization (Trial registration No. ChiCTR-ONC-17010498).

Aspirin modulates the inflammatory response in a thrombus­stimulated LMVEC model.

The purpose of the present study was to examine whether aspirin interferes with the inflammatory response in a thrombus­stimulated lung microvascular endothelial cell (LMVEC) model. The LMVECs were randomly divided into eight groups: Normal group (group N), model group (group M), model + ASP group (group M+A), model+CX3CL1­short hairpin (sh)RNA group (group M+SH), model + CX3CL1­overexpression vector group (group M+CX3), model + ASP + shRNA group (group M+A+SH), model + ASP + CX3CL1­overexpression vector group (group M+A+CX3), and normal + virus control group (group N+V). The endothelial cells were cultured, and a thrombus was added to the cells. Briefly, 12 h following the precipitation of the thrombus, data from ELISA, reverse transcription­quantitative polymerase chain reaction analysis and confocal microscopy revealed that the levels of tumor necrosis factor (TNF)­α, interleukin (IL)­6, CX3C chemokine ligand 1 (CX3CL1), CX3C chemokine receptor 1 (CX3CR1) and nuclear factor­κB (NF­κB) in group M were increased, compared with those in group N (P<0.01). These levels, with the exception of TNF­α, were significantly lower in group M+SH, compared with those in group M (P<0.01). Furthermore, the levels of IL­6 in groups M+A, M+CX3 and M+A+CX3 were decreased, compared with those in group M (P<0.01); the level of TNF­α in group M+A+SH was decreased, compared with that in group M (P<0.01); the level of CX3CR1 waslower in groups M+A and M+A+SH, compared with that in group M (P<0.01), and the level of NF­κB in group M+SH was decreased, compared with the level in group M and group M+A (P<0.05). In conclusion, the thrombus­stimulated LMVEC model exhibited induced production of TNF­α, IL­6, CX3CL, CX3CR1, NF­κB and intercellular adhesion molecule­1. Furthermore, it was confirmed that the signaling pathways involving CX3CL1­NF­κB, IL­6 and TNF­α were partly inhibited by aspirin.

Urokinase Attenuates Pulmonary Thromboembolism in an Animal Model by Inhibition of Inflammatory Response.

Inflammatory response is an important determining factor for the mortality of patients with pulmonary thromboembolism. Inflammatory mediators can promote thrombus formation and increase hemodynamic instability. Urokinase is a commonly used drug for the treatment of PTE. The effect of urokinase on inflammatory reaction in PTE is still unclear. Our study was aimed at evaluating the effects of the intervention of urokinase and urokinase combined with aspirin in PTE rats. Results revealed that a large amount of infiltrated inflammatory cells surrounding the bronchus, vessels, and pulmonary mesenchyme, and even pulmonary abscess were observed in the PTE rats. CX3CL1/CX3CR1 coexpression, CX3CL1/NF-κB coexpression, and TXA2 were significantly higher. After treatment with urokinase, pulmonary embolism was partially dissolved and inflammatory cell infiltration was significantly reduced. The expression of TNNI3, BNP, D2D, PASP, PADP, PAMP, and TXA2, as well as CX3CL1/CX3CR1 coexpression and CX3CL1/NF-κB coexpression were significantly lowered. Aspirin showed no synergistic action. Therefore, these findings suggested the occurrence of inflammation during the process of PTE in rats. Urokinase treatment reduced the inflammatory response.

Electroacupuncture improves acute bowel injury recovery in rat models.

Electroacupuncture (EA) accelerates intestinal functional recovery in sepsis. The present study investigated ghrelin and ghrelin receptor (GSH-R) levels during EA in rats with acute bowel injury (ABI). Rats were grouped into four groups: Sham, ABI, ABI+EA and ABI+GHRA+EA (n=12 per group). ABI was induced by cecal ligation and puncture (CLP). EA on bilateral Zusanli acupoints was performed following CLP. GSH-R blocker (GHRA) was used following CLP but prior to EA for ABI+GHRA+EA rats. Rats were sacrificed 12 h following CLP. Serum ghrelin, tumor necrosis factor-α (TNF-α) and high mobility group box 1 (HMGB1) levels, as well as ghrelin and GSH-R protein expression, water content, pathological changes and myeloperoxidase (MPO) and diamine oxidase (DAO) activities in the bowel tissues, were measured. ABI rats, compared with the sham rats, had significantly lower levels of ghrelin and GSH-R in the serum and bowel tissue, and higher Chiu's score (all P<0.05). The ABI+EA rats, compared with the ABI rats, had significantly reduced serum TNF-α and HMGB1 levels, bowel water content, MPO activity and Chiu's score (all P<0.05), and significantly higher serum ghrelin (121.2±10.7 vs. 86.7±6.4 pg/ml), bowel ghrelin (0.12±0.02 vs. 0.08±0.01), GSH-R (0.05±0.04 vs. 0.03±0.01) and DAO activity (18.74±4.18 vs. 13.52±2.33 U/ml; all P<0.05), indicating an improvement of the intestinal mucosal barrier. GHRA reversed the protective effects of EA. Therefore, EA improved ABI recovery by promoting ghrelin secretion and upregulating GSH-R expression.

[Advances in risk factors of Klebsiella pneumoniae carbapenemases-producing Klebsiella pneumoniae infection or colonization and its treatment strategies].

OBJECTIVE: Klebsiella pneumoniae carbapenemases-producing Klebsiella pneumoniae (KPC-Kp) has caused a global public health crisis, and the severity of its infection is associated with high mortality in hospitalized patients. Therefore, the KPC-Kp prevention methods and the corresponding treatment strategy exploration are imminent. The risk factors and the treatment progress of KPC-Kp colonization or infection are reviewed in this paper to explore corresponding preventive measures and treatment strategies for clinical prevention and treatment.