From 1975 to 1976,in Linxian county of Henan province,52 patients with early stage easophageal carcinoma were treated by radiotherapy alone. After 10-year follow-up, the 5-and 10-year surving rates were 73.1%(38/52) and 50.0%(56/52), respectively. Local recurrence was considered as the major cause of death and distance metastasis as the minor. We believe that it is very important to do the "three early "(find early, diagnose early and treat early ) and D T5000～5500cGy/5～5.5wks may be the best dose for radiotherapy alone for early easophageal carcinoma.

Objective To describe the monitoring and control of pan-drug resistant Acinetobacter baumannii (XDRABA) colonization and infection in a medical intensive care unit (ICU),and to summarize the effective measures of surveillance of nosocomial infection and control.Methods Nonsurgical patients admitted to medical ICU of Peking University People's Hospital from September 2009 to April 2013 with length of ICU stay over 48 hours were surveyed.Number of cases of colonization and infection of XDRABA per month was recorded,and the clinical features of patients with XDRABA colonization and infection were observed.The control of XDRABA colonization and infection was divided into three stages:① Outbreak stage,from September 2009 to August 2010,the infection control measures included stringent hand hygiene and surface disinfection,use of disposable ventilator tubes and improvement in antibiotics use.② Environmental control stage,from September 2010 to April 2012,the infection control measures consisted of on-the-spot investigation,isolation of patients with XDRABA colonization and infection,tubes terminal environment disinfection.③ Microbial screening stage,from May 2012 to April 2013,throat,nose and axillary swabs were obtained when the patients admitted.Results From 2009 September to 2013 April there was a total of 193 patients colonized or infected with XDRABA,and 64 patients died (mortality rate was 33.2％),and 133 (68.9％) patients were on mechanical ventilation.Patients with XDRABA colonization and infection had severer illness [acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ) score 20.3 ±6.7],longer ICU stay [(34.6 ± 13.8) days].In outbreak stage,number of cases with XDRABA colonization and infection was 5-9 per month.In environmental control stage,case number of XDRABA colonization and infection was 3-6 per month.In microbial screening stage,case number of XDRABA colonization and infection,which were already present,was 2-4 per month,and they were mainly admitted from emergency department (59.5％).The number of cases of ICU acquired XDRABA colonization and infection decreased from 2-3 to 0-1 per month.Conclusion To control the colonization and infection of XDRABA,monitoring of microorganism,hand hygiene,isolation of patients with XDRABA colonization and infection,and stringent environment disinfection were very necessary.

Objective To investigate the clinical features and risk factors on outcomes of patients with cardio-renal syndrome (CRS) in surgical intensive care unit (SICU). Methods The clinical data of the patients admitted to SICU of Peking University People's Hospital from January 1st 2017 to December 31st 2017 were analyzed retrospectively, including gender, age, severity of the disease, underlying diseases, type of CRS, precipitating factors of CRS, cardiac and renal function [cardiac troponin I (cTnI), B-type natriuretic peptide (BNP), serum creatinine (SCr), glomerular filtration rate (eGFR)], outcomes [secondary outcomes, duration of mechanical ventilation, the length of ICU stay, the length of hospital stay, 28-day mortality and hospital mortality]. Patients were grouped according to CRS classification or hospitalization prognosis, the clinical features within different CRS types were analyzed, and risk factors on outcomes of the CRS patients were analysed by Logistic regression. Results 86 (7.3%) of the 1 172 patients during the study period had CRS. ①CRS clinical features: CRS 1-5 type patients accounted for 24.4% (21 cases), 1.2% (1 case), 20.9% (18 cases), 1.2% (1 case) and 52.3% (45 cases) respectively, CRS type 1, 3 and 5 were the main types (i.e. acute cardiac and renal dysfunction), while type 5 CRS was the highest (i.e. organ dysfunction caused by simultaneous involvement of cardiac and renal functions secondary to systemic diseases was the most common). Baseline BNP (Z = 11.365, P =0.023), SCr peak (Z = 13.405, P = 0.009) and baseline eGFR (F = 2.648, P = 0.037) were significantly different within the CRS 5 types. The basic cardiac function of type 1 CRS patients was significantly worse than that of type 3 and type 5 CRS patients [baseline BNP (μg/L): 434.2 (187.0, 1 252.0) vs. 154.9 (66.4, 272.5), 268.5 (124.1, 486.6), both P <0.05]. The basic renal function of type 3 CRS patients was significantly worse than that of type 5 CRS patients [baseline eGFR (mL/min): 71.0±30.3 vs. 88.3±29.0, P < 0.05]. The severity of acute kidney injury (AKI) in type 3 CRS patients was significantly higher than that in type 1 and type 5 CRS patients [SCr peak (μmol/L): 285.0 (171.5, 420.6) vs. 143.0 (99.5, 213.5), 189.0 (105.5, 280.5), both P < 0.01]. There were no significant differences in gender, age, department, acute physiology and chronic health evaluationⅡ (APACHEⅡ), intraoperative blood loss, basic cTnI and SCr levels, BNP peak, AKI staging and prognostic indicators among patients with various types of CRS. ② Death risk analysis:43 (50%) of the 86 CRS patients died during the hospital stay. Compared with the survival patients, CRS death patients were older [years old: 72 (57, 80) vs. 62 (50, 73)] and had higher APACHEⅡ score [22 (17, 29) vs. 18 (15, 21)], with higher proportion of cerebrovascular disease (9.3% vs. 0). Regarding to precipitating factors of CRS, sepsis/septic shock (41.9% vs. 18.6%) and surgery stress (9.3% vs. 0) were remarkably increased in death patients. Death patients had higher cTnI and SCr peak [cTnI peak (μg/L): 1.155 (0.192, 5.125) vs. 0.122 (0.045, 0.610), SCr peak (μmol/L): 208 (143, 295) vs. 146 (101, 289)] and also high proportion of AKI stage 3 (41.9% vs. 20.9%), higher rate of secondary infection (67.4% vs. 30.2%), prolonged duration of mechanical ventilation and the length of ICU stay [hours: 179 (61, 470) vs. 37 (7, 134);days: 10 (4, 24) vs. 5 (2, 11)], with statistically significant differences (all P < 0.05). Logistic regression analysis showed that the elderly [odds ratio (OR) = 1.053, 95% confidence interval (95%CI) = 1.003-1.094, P = 0.010], high APACHE Ⅱscore (OR = 1.165, 95%CI = 1.057-1.285, P = 0.002), sepsis/septic shock (OR = 4.561, 95%CI = 1.351-15.391, P = 0.014) and AKI stage 3 (OR = 5.468, 95%CI = 1.457-20.530, P = 0.012) were independent risk factors for hospital death in CRS patients. Conclusions Surgical ICU patients with CRS are characterized by acute cardiac and renal dysfunction. CRS type 5 is the most common and has a high fatality rate. Age, severity of illness, sepsis/septic shock and AKI stage 3 are independent risk factors of death.

Objective: To explore the role of the low-affinity A2b adenosine receptors (Adora2b) in pulmonary microvascular endothelial inflammation induced by lipopolysaccharide and its mechanism. Methods: Rat pulmonary microvascular endothelial cells (PMVECs) were isolated and cultured in vitro. After serum deprivation for 24 hours, cells were pretreated with Adora2b specific agonist BAY60-6583 (0.1, 1, 10 μmol/L) or Adora2b specific antagonist PSB1115 (1 μmol/L) for 1 hour, respectively, and then challenged with LPS (100 μg/L). Cells without treatment were served as the control group, and those treated with LPS, BAY60-6583 or PSB1115 alone were served as single challenge groups. After incubation with specific drugs for 24 hours, the apoptosis of PMVECs was analyzed by flow cytometry using Annexin V/propidium iodide (PI) technique. The levels of early inflammatory factors in cultured medium were measured using enzyme linked immunosorbent assay (ELISA). The mRNA expressions of chemotactic factors and adhesion molecules were determined by real-time quantitative-polymerase chain reaction (RT-qPCR). Polymorph nuclear neutrophils (PMNs) from venous blood of healthy rats were isolated, and PMN migration through PMVECs monolayer under stimulation of drugs was observed in transwell inserts. The monolayer permeability of PMVECs after adhesion of PMNs was determined by fluorescein isothiocyanate (FITC)-albumin assay. Oxidative stress was detected by DCFH-DA assay. Results: Compared with the control group, more cells entered into the apoptosis stage after LPS challenge. Meanwhile, the levels of interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in cultured medium were significantly increased, as well as the mRNA expressions of chemotactic factors [C-X-C motif chemokine ligand 1 (CXCL-1), CXCL-3 and monocyte chemoattractant protein-1 (MCP-1)] and adhesion molecules [E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)]. More PMNs migrated through PMVECs following adhesion and the monolayer permeability of PMVECs was rapidly enhanced. The oxidative stress was upregulated. Compared with LPS group, BAY60-6583 pretreatment could dose-dependently decrease the rate of apoptosis, attenuate trans-endothelial migration of PMNs and decrease the endothelial cell barrier leakage. There were significant differences even after incubation of 0.1 μmol/L BAY60-6583 [apoptosis rate: (21.12±2.12)% vs. (27.66±3.57)%, number of migrated PMNs/HP: 260.60±18.24 vs. 290.20±16.48, permeability coefficient (Pd, ×10^-6 cm/s): 28.28±2.04 vs. 32.55±2.13, all P < 0.05]. Meanwhile, BAY60-6583 pretreatment also downregulated the levels of early proinflammatory factors in a dose-dependent manner as well as the mRNA expressions of chemotactic factors and adhesion molecules. The statistic difference was significant while treated with 1 μmol/L BAY60-6583 [IL-1β (ng/L): 475.75±63.15 vs. 755.25±67.42, TNF-α (ng/L): 560.25±69.96 vs. 818.75±60.92, CXCL-1 mRNA (2^-ΔΔCt): 3.57±0.28 vs. 5.27±0.69, CXCL-3 mRNA (2^-ΔΔCt): 4.56±0.48 vs. 7.32±0.54, MCP-1 mRNA (2^-ΔΔCt): 2.21±0.31 vs. 3.35±0.21, E-selectin mRNA (2^-ΔΔCt): 4.64±0.09 vs. 7.28±0.73, ICAM-1 mRNA (2^-ΔΔCt): 4.14±0.30 vs. 5.89±0.25, VCAM-1 mRNA (2^-ΔΔCt): 2.23±0.19 vs. 2.92±0.33, all P < 0.05]. Furthermore, pretreatment of 10 μmol/L BAY60-6583 could decrease the oxidative stress [reactive oxygen species (RFU): 629.05±33.10 vs. 781.45±64.59, P < 0.05]. Contrast, PSB1115 pretreatment aggravated apoptosis of PMVECs after LPS incubation [(34.36±4.57)% vs. (27.66±3.57)%], upregulated expressions of proinflammatory and chemotactic factors as well as adhesion molecules [IL-1β (ng/L): 889.00±63.11 vs. 755.25±67.42, TNF-α (ng/L): 939.00±43.44 vs. 818.75±60.92, CXCL-1 mRNA (2^-ΔΔCt): 6.66±0.65 vs. 5.27±0.69, CXCL-3 mRNA (2^-ΔΔCt): 10.42±0.51 vs. 7.32±0.54, MCP-1 mRNA (2^-ΔΔCt): 4.85±0.34 vs. 3.35±0.21, E-selectin mRNA (2^-ΔΔCt): 8.42±0.47 vs. 7.28±0.73, ICAM-1 mRNA (2^-ΔΔCt): 7.46±0.72 vs. 5.89±0.25, VCAM-1 mRNA (2^-ΔΔCt): 4.35±0.26 vs. 2.92±0.33], aggravated trans-endothelial migration of PMNs (cells/HP: 348.40±22.68 vs. 290.20±16.48), enhanced the leakage of PMVECs monolayer [Pd (×10^-6 cm/s): 39.65±2.69 vs. 32.55±2.13] and increased oxidative stress in PMVECs [reactive oxygen species (RFU): 847.04±29.26 vs. 781.45±64.59], with statistically significant difference (all P < 0.05). Conclusion Activation of endothelial Adora2b attenuates LPS-induced pulmonary microvascular inflammation by decreasing the release of early inflammatory factors, downregulating expressions of chemotactic factors and adhesion molecules, attenuating trans-endothelial migration of PMNs and oxidative stress in PMVECs, which suggest endothelial Adora2b is apotential anti-inflammatory target in the treatment of LPS-induced acute lung injury.

Objective To discuss the value of pregnantal ultrasonography(US) on fetus' complicate congenital heart diseases(CHD). Methods The uhrasonographic fetures of fetus complicate CHD were analyzed and compared with the pathological diagnosis. Resells Twenty fetus' complicate CHD were diagnosed by pregnantal US. Four cases with single ventricle, two eases with transposition of great arteries,two eases with double outlet right ventricle,two cases with truncus arteriosus,three cases with hypoplastic left heart syndrome, three cases with endocardial cushion defect, two cases with hypoplastic right heart syndrome,one case with tetralogy of Fallot and one case with pulmonary atresia were included. The diagnosing according rate was 100%. Conclusions Pregnantal US can fully evaluate the fetus' complicate CHD.

Objective To explore the role of the A2b adenosine receptor (Adora2b) in lipopolysaccharide (LPS)-induced injury of human pulmonary microvascular endothelial cells (HPMECs), and its mechanism. Methods HPMECs were cultured in vitro. The LPS dose-effect experiment, time-effect experiment and the Adora2b agonist/antagonist intervention experiment were performed respectively. ① Dose-effect and time-effect experiments: HPMECs were stimulated with 1, 10, 100, 1 000 μg/L LPS for 24 hours, or 100 μg/L LPS for 4, 8, 12, 16, 24 hours. Cell viability was measured by cell counting kit-8 (CCK8). The protein and mRNA expressions of Adora2b were determined by Western Blot and real-time reverse transcription-polymerase chain reaction (RT-PCR) respectively. ② Adora2b agonist/antagonist intervention experiment: serum-starved HPMECs were pretreated with Adora2b specific agonist BAY60-6583 (0.1, 1, 10 μmol/L) or Adora2b specific antagonist PSB1115 (1 μmol/L) for 1 hour, respectively, and then incubated with 100 μg/L of LPS for 24 hours. The HPMECs without treatment were served as blank control group, and those treated with LPS, BAY60-6583 or PSB1115 alone were served as single challenge groups. The monolayer permeability of HPMECs was determined by fluorescein isothiocyanate (FITC)-dextran. Cell cycle was analyzed by flow cytometry. The mRNA expressions of VE-cadherin, occludin, vascular endothelial growth factor (VEGF) and angiopoietin-1 (ANGPT1) were determined by RT-PCR. Results ① Dose-effect and time-effect experiments: LPS induced the decreased cell viability of HPMECs in dose and time-dependent manner. Compared with the control group, the protein expression of Adora2b was sharply up-regulated after 100 μg/L or 1 000 μg/L LPS stimulation. Meanwhile, LPS was shown to cause a dose and time-dependent induction of Adora2b transcript level. ② Adora2b agonist/antagonist intervention experiments: compared with the control group, the monolayer permeability of HPMECs was rapidly enhanced after LPS treatment, and lower cell viability and proliferation, as well as the expression of cell junction and angiogenic factors were downregulated. Compared with LPS group, 0.1, 1, 10 μmol/L BAY 60-6583 pretreatment could decrease the endothelial cell barrier leakage in a dose-dependent manner [Pd: (203.06±15.24)%, (164.15± 17.82)%, (125.69±10.38)% vs. (218.53±12.05)%], and promote cell proliferation of HPMECs [the proportion of S and G2 phases: (24.36±1.40)%, (32.37±0.95)%, (40.05±2.99)% vs. (18.83±0.73)%]. Pretreatment of 10 μmol/L BAY60-6583 also upregulated the mRNA expressions of cell junction and angiogenic factors [VE-cadherin (2-ΔΔCt):2.17±0.23 vs. 0.56±0.10, occludin (2-ΔΔCt): 5.32±0.28 vs. 0.48±0.11, VEGF (2-ΔΔCt): 4.44±0.34 vs. 0.58±0.09, ANGPT-1 (2-ΔΔCt): 5.98±0.73 vs. 0.66±0.10, all P < 0.01]. PSB1115 pretreatment aggravated injury of microvascular endothelial cells after LPS incubation, with lower cell viability, slower proliferation and less expression of VEGF and ANGPT1. There was no influence of BAY 60-6583 or PSB1115 single treatment on cell viability, cell cycle and the expression of angiogenic factors in HPMECs. Conclusions In vitro studies of cultured HPMECs exposed to LPS are identified as dose and time-dependent induction of Adora2b transcript and corresponding protein induction. Activation of Adora2b attenuates LPS-induced pulmonary microvascular endothelial cell barrier enhancement by regulating intercellular junction and promoting angiogenesis, suggesting Adora2b as potential therapeutic target in the treatment of LPS-induced forms of acute lung injury.

OBJECTIVE: To explore the causes and the management of serious eye complications occurring in the endoscopic sinus surgery. METHOD: Three patients of chronic sinusitis and nasal polyps suffered with blindness in endoscopic sinus surgery and in nasal packing with iodoform and petrolatum gauze were treated. RESULT: Orbital wall and structure were injured in 2 cases during endoscopic sinus surgery, among which, 1 case blinded with deformation of the eyeball during operation underwent optic nerve exploration and orbital muscle reparation immediately. One case developed periocular swelling, eyelid hematoma, conjunctiva edema and blinded 2 days later, and was treated with hematoma clearance and optic nerve decompression. Another 1 case blinded immediately after ethmoid packing, and vision recovered after nasal pack removed. Antibiotics, corticosteroid and nerve growth factor were administered for 4 weeks in all patients. After 6-month follow-up, 1 case was blinded with eyeball atrophy, 1 case was only photonasty, another regained normal vision. CONCLUSION The causes of blindness in endoscopic sinus surgery are directly related to orbital structure trauma and orbital hematoma. The optic nerve during operation should be protected carefully, if ethmoid sinus over development is demonstrated by CT scan. The application of gauze should be avoided when the medial orbital wall is injured. Decompression of optic nerve should be performed as early as possible, if vision damaged.
Adult ; Blindness ; etiology ; prevention & control ; Endoscopy ; adverse effects ; Female ; Humans ; Male ; Middle Aged ; Nose ; surgery ; Otorhinolaryngologic Surgical Procedures ; adverse effects ; Postoperative Complications ; prevention & control

OBJECTIVE: To enhance the safety of nasal endoscopic surgery and decrease its complications of eyes. METHOD: Three patients of chronic rhinosinusitis and nasal polyposis with lipogranulomas of the eyelids after nasal endoscopic surgery and nasal packing of petrolatum gauze were reported and analyzed, and their treatment results were presented during the last 2 years. RESULT: The medial orbital wall injury occurred in all three patients during endoscopic sinus surgery. The patients developed an ipsilateral periocular swelling, eyelid hematoma and palpebral conjunctival edema during 2 to 3 hours after surgery. Nasal packs petrolatum gauze were removed 10-24 hours after surgery. The patients were discharged from hospital when periorbital swelling and eyelid ecchymoma disappeared, and nasal cavity obstruction was improved 6 to 8 days after surgery. The swelling and nodular mass of ipsilateral eyelids (one in left upper eyelid and two in right lower eyelid) were found 12-15 days after surgery, and their eye movement and eyesight were normal. Antibiotic and corticosteroid were administered for 3 4 weeks with only improvement in eyelid swelling. These masses of eyelids were completely excised through palpebral margin 1-6 months after surgery. The histopathological examination of the surgical specimens showed lipogranuloma. No recurrence and symptom of the eyes had been observed during 4-18 months follow up. CONCLUSION The lipogranuloma of the eyelid is a rare and late complication after nasal endoscopic surgery and nasal packing with vaspetrolatum gauze. The medial orbital wall injury and bleeding during surgery, and vaseline of nasal packing permeated into the eyelid are the direct causes of this complication. The application of petrolatum gauze should be avoided when the medial orbital wall trauma is identified. The complete excision of granulomas is a best effective therapy.
Adult ; Endoscopy ; adverse effects ; Eyelid Diseases ; diagnosis ; etiology ; therapy ; Female ; Granuloma ; diagnosis ; etiology ; therapy ; Humans ; Male ; Middle Aged ; Postoperative Complications ; diagnosis ; therapy

Objective: To analyze the risk factors related to the myocardial injury after non-cardiac surgery (MINS) in patients who underwent major abdominal surgery. Methods: The clinical data of all patients admitted in the surgical ICU of Peking University People′s Hospital from Jan 2016 to Dec 2018 were analyzed. Logistic multivariate analysis was performed to analyze the association of clinical characteristics with the incidence of MINS. Results: A total of 322 patients were included, 48.4% (156/322) were diagnosed as with MINS. 97.4% (152/156) of MINS occurred during the first 72 h of admission. Multivariate analysis showed that independent predictive factors of MINS were age >65y (OR=1.747, P=0.021), body mass index (OR=1.085, P=0.008), acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ, OR=1.066; P=0.047), hypertension (OR=1.747, P=0.027), blood lactate (OR=1.393, P=0.001) and acute kidney injury (OR=2.065, P=0.047). Conclusions The incidence of MINS in patients who underwent major abdominal surgery was high. Age, body mass index, APACHE Ⅱ score, hypertension, blood lactate level and acute kidney injury after surgery were independent risk factors of MINS.