From the Cover: Proton transfers are key elementary steps in ethylene polymerization on isolated chromium(III) silicates

Mononuclear Cr(III) surface sites were synthesized from grafting [Cr(OSi(O^tBu)₃)₃(tetrahydrofurano)₂] on silica partially dehydroxylated at 700 °C, followed by a thermal treatment under vacuum, and characterized by infrared, ultraviolet-visible, electron paramagnetic resonance (EPR), and X-ray absorption spectroscopy (XAS). These sites are highly active in ethylene polymerization to yield polyethylene with a broad molecular weight distribution, similar to that typically obtained from the Phillips catalyst. CO binding, EPR spectroscopy, and poisoning studies indicate that two different types of Cr(III) sites are present on the surface, one of which is active in polymerization. Density functional theory (DFT) calculations using cluster models show that active sites are tricoordinated Cr(III) centers and that the presence of an additional siloxane bridge coordinated to Cr leads to inactive species. From IR spectroscopy and DFT calculations, these tricoordinated Cr(III) sites initiate and regulate the polymer chain length via unique proton transfer steps in polymerization catalysis.Almost half of the world’s high-density polyethylene is produced by the Phillips catalyst, a silica-supported chromium oxide (CrO_x/SiO₂) (1). This catalyst is prepared by incipient wetness impregnation of a chromium salt on silica, followed by high temperature calcination. Contacting this material with ethylene forms the active reduced species in situ that polymerizes ethylene. The Phillips catalyst is active in the absence of activators that are typically required for polymerization catalysts (2). Despite 50 y of research, the catalytically active site and the initiation mechanism, particularly the formation of the first Cr–C bond, remain controversial. Numerous spectroscopic techniques [infrared (IR), ultraviolet-visible (UV-Vis), electron paramagnetic resonance (EPR), X-ray absorption spectroscopy (XAS), etc.] established that the Phillips catalyst contains a complex mixture of surface Cr species, of which only ∼10% are active in polymerization (3, 4). The low number of active sites is one of the main limiting factors in using spectroscopic methods to study this material because the spectroscopic signature mainly belongs to inactive species.Previous molecular approaches to determine the Phillips catalyst ethylene polymerization mechanism focused on systems containing preformed Cr–C bonds (5–7). We recently reported the preparation of well-defined silica-supported Cr(II) and Cr(III) dinuclear sites (8), where Cr(III) species are active polymerization sites, in contrast to Cr(II), which is consistent with extensive research on homogeneous chromium complexes (9–11). We proposed that these well-defined Cr(III) silicates initiate polymerization by the heterolytic cleavage of a C–H bond of ethylene on a Cr–O bond to form a Cr–vinyl species that is capable of inserting ethylene by a Cossee–Arlman mechanism (8). However, extensive studies on Phillips catalyst invoke mononuclear polymerization sites (12–18). Furthermore, direct evidence of the active site structure and the polymerization mechanism is critically needed. Here we investigate the preparation and the detailed characterization of isolated Cr(III) sites supported on silica, prepared by grafting [Cr^III(OSi(O^tBu)₃)₃(tetrahydrofurano; THF)₂] (19) on dehydroxylated silica and a subsequent thermal treatment under vacuum. These isolated Cr(III) sites are highly active in ethylene polymerization in the absence of coactivator. Computational investigations in combination with IR spectroscopy indicate that polymerization occurs on tricoordinate Cr(III) sites and involves two key proton transfer steps: (i) formation of the first Cr–C bond through the C–H activation of ethylene across a Cr–O bond and (ii) termination by the microreverse of the initiation step while chain growth occurs by classical Cossee–Arlman insertion polymerization (20, 21).     

Deoxygenation of the Baltic Sea during the last century

Deoxygenation is a global problem in coastal and open regions of the ocean, and has led to expanding areas of oxygen minimum zones and coastal hypoxia. The recent expansion of hypoxia in coastal ecosystems has been primarily attributed to global warming and enhanced nutrient input from land and atmosphere. The largest anthropogenically induced hypoxic area in the world is the Baltic Sea, where the relative importance of physical forcing versus eutrophication is still debated. We have analyzed water column oxygen and salinity profiles to reconstruct oxygen and stratification conditions over the last 115 y and compare the influence of both climate and anthropogenic forcing on hypoxia. We report a 10-fold increase of hypoxia in the Baltic Sea and show that this is primarily linked to increased inputs of nutrients from land, although increased respiration from higher temperatures during the last two decades has contributed to worsening oxygen conditions. Although shifts in climate and physical circulation are important factors modulating the extent of hypoxia, further nutrient reductions in the Baltic Sea will be necessary to reduce the ecosystems impacts of deoxygenation.Dead zones are hypoxic (low-oxygen) areas unable to support most marine life, and over the past 50 y they have spread rapidly in the open ocean (1) as well as in coastal ecosystems (2). Global warming is thought to be a major driver for these changes (3), although biogeochemical factors have also been recognized, especially in coastal marine ecosystems (4, 5). In the Baltic Sea, the present spread of hypoxia is the combined result of climate changes influencing deepwater oxygenation (6) and increased eutrophication (7, 8), resulting in a hypoxic area ranging between 12,000 and 70,000 km² with an average of 49,000 km² over the time period 1961–2000 (7). Here, we separate the effects of the two factors on oxygen conditions.Physical factors are an important consideration in whether an ecosystem will experience hypoxia. The Baltic Sea is naturally prone to hypoxia due to a restricted water exchange with the ocean and a long residence time above 30 y (9, 10). Saltier, denser water from the North Atlantic flows over a series of shallow sills in the Danish Straits to ventilate waters below the permanent halocline and are governed by meteorological-induced variations in sea levels (11), displaying variations at decadal scales (12, 13). The dense saltwater inflows bring new supplies of oxygen to bottom waters, but at the same time enhance stratification, creating larger bottom areas that experience hypoxia (14). In particular, the ventilation of the deeper waters is attributed to events of larger inflows of high-saline water (>17), termed Major Baltic Inflows (MBIs), that have been less frequent in the last three decades (6).Climate warming decreases oxygen solubility due to higher water temperature, increases stratification, and enhances respiration processes (15). Climate warming is likely to be accompanied by increased precipitation and inflows of freshwater and nutrients to coastal waters in many areas of the globe. Increasing nutrient inputs from land stimulates primary production and export of organic material to the deep waters, thereby disrupting the subtle natural balance between oxygen supply from physical processes and oxygen demand from consumption of organic material. However, the importance of decreasing oxygenation versus increasing nutrient inputs for explaining the recent spread of hypoxia is not known (6, 7).Water column measurements of dissolved oxygen concentrations began around 1900 with more regularly spaced measurements commencing in the 1960s (Fig. S1), allowing a more consistent assessment of the spatial extent of hypoxia (7, 14). The sparse temporal and spatial resolution of oxygen data before 1960 allowed only assessing hypoxia at specific locations (16) or specific years (17). To our knowledge, our study is the first to report basin-wide trends of stratification and oxygen conditions from 1898 to present, and here we will focus on the two basins that have perennial hypoxia—the Bornholm Basin and the Gotland Basin (Fig. S2). These two basins are connected via a channel with a sill depth of 60 m.     

丙肝相关性肝癌根治术后复发规律及危险因素分析

目的：分析丙肝相关性肝癌（HCV-HCC）根治术后复发规律及相关危险因素,探讨针对复发时相的个体化临床干预。 方法：回顾98例行HCV-HCC根治术的患者临床病理资料,分析患者根治术后复发规律,对复发的可能影响因素进行单因素及多因素分析,并对病毒因素进行分层分析。 结果：全组根治术后有2个复发高峰,以24个月为界分为早、晚期;COX比例风险模型分析显示,肿瘤低分化、镜下微血管侵犯为术后早期复发的独立危险因素（P<0.001）,病毒载量为晚期复发的独立危险因素（P=0.013）;术后病毒载量持续阴性患者无瘤生存期明显长于术后持续高病毒载量或病毒载量不稳定者（P<0.001）。 结论：HCV-HCC根治术后早、晚期复发影响因素不同;早期复发率较高,预防性TACE可改善早期复发高危者预后;术后抗病毒治疗可改善远期疗效。

     

癌性胸水胸腔热化疗对淋巴细胞亚群变化的临床意义

目的研究癌性胸水胸腔持续灌注热化疗对淋巴细胞亚群的变化。方法在全麻下对21例癌性胸水患者,内置二根胸管,出胸水管连接水封瓶,经过人工心肺机的灌注泵,接上铝制螺纹管(变温用),连接进胸水管入胸腔,向胸水中加入化疗药物顺铂200~250 mg/m2,保持胸水温度42~45℃,持续灌注60 m in左右,于术前、术后第3、7 d、2周分别作淋巴细胞亚群测定,以了解胸腔热化疗对免疫功能的影响。结果热化疗后CD19、CD25的表达率明显增高(P<0.05和<0.01)。结论胸腔持续灌注热化疗使癌性胸水缓解率明显提高,是一种安全、有效的治疗癌性胸水的好方法,而且能使B淋巴细胞免疫功能及T淋巴细胞活化率明显提高。     

与护理有关的医疗纠纷原因分析及其对策

对21所医疗机构与护理有关的医疗纠纷发生情况进行调查分析.结果 发现与护理有关的医疗纠纷案件增多,医疗事故争议诉讼案件显著增长,争议补(赔)偿数额明显增加.提出与护理有关的医疗纠纷发生原因包括医院管理方面、护理人员方面、患者方面及社会因素等;需要采取完善医院管理、提高护理人员自身防范意识、加强医护惠三方沟通及树立良好社会形象等措施加以防范.     

一氧化氮和前列腺素在门静脉高压性胃病大鼠胃粘膜灌注中的作用

目的 探讨一氧化氮（NO）和前列腺素在门静脉高压性胃病（PHG）大鼠胃粘膜灌注中的作用。方法 部分结扎大鼠门静脉主干2周后,采用中性红清除率法测定大鼠胃粘膜血流量（GMBF）,同时观察门静脉压力（PVP）的变化。结果 PHG组大鼠GMBF和PVP显著高于假手术组（t=3.431、3．312,P＜0．01）。低剂量的NO合成酶抑制剂L－硝基－精氨酸甲酯（L－NAME）呈剂量依赖性降低PHG大鼠GMBF,而对假手术组GMBF无明显影响;高剂量的L－NAME（12mg/kg)能非常显著降低PHG和假手术组大鼠GMBF。前列腺素环氧合酶抑制剂消炎痛能明显降低PHG组大鼠GMBF,而对假手术组GMBF无明显影响;预先给消炎痛处理后在假手术组大鼠中,静脉注射低剂量L－NAME（4mg/kg)前后GMBF无明显变化,高剂量L－NAME（12mg/kg)降低大鼠的GMBF与未用消炎痛处理组比无明显变化;预先给消炎痛处理后在PHG组大鼠中,L－NAME剂量（4mg/kg、12mg/kg)依赖性降低大鼠的GMBF与未用消炎痛处理组比无明显改变。结论 NO、前列腺素在调节PHG大鼠的GMBF起重要作用,但两者无协同作用。     

双源CT联合血清CRP水平检测对痛风性关节炎的诊断价值

目的 探讨双源CT联合血清C反应蛋白（CRP）水平检测对痛风性关节炎的诊断价值。方法 选择本院2018年1月—2022年3月收治的166例疑似痛风性关节炎患者,分为痛风性关节炎组与非痛风性关节炎组行双源CT及血清CRP水平检测,以美国风湿病协会（ACR）制定的痛风性关节炎诊断标准明确痛风性关节炎诊断,计算双源CT及血清CRP单独与联合诊断痛风性关节炎的效能并分析其临床价值。结果 共有126例患者（75.90%）明确痛风性关节炎诊断。痛风性关节炎组双源CT图像绿色结晶检出率高于非痛风性关节炎组,差异有统计学意义（P＜0.05）。痛风性关节炎组血清CRP水平高于非痛风性关节炎组（P＜0.05）,但两组血清CRP阳性率比较,差异无统计学意义（P＞0.05）。双源CT联合血清CRP诊断痛风性关节炎的特异性、准确率、阳性预测值、阴性预测值均高于单项诊断,差异有统计学意义（P＜0.05）。结论 双源CT联合血清CRP水平检测能够为痛风性关节炎的无创诊断提供可靠参考     

CD44v6、E-cadherin和nm23-H1在子宫颈癌中的表达及意义

目的:探讨CD 44V 6、E-cadherin和nm 23-H 1蛋白表达与子宫颈癌的发生、发展及转移的关系。方法:采用免疫组化SP法检测50例子宫颈癌组织和10例正常子宫颈组织中CD 44v6、E-cadherin和nm 23-H 1蛋白的表达情况。结果:CD 44v6蛋白在子宫颈癌组织中的阳性率为66%,CD 44v6高表达与宫颈癌的组织学分级、淋巴结转移呈正相关(P<0.05及P<0.01)。E-cadherin和nm 23-H 1蛋白在宫颈癌组织中阳性表达率分别为62%和48%,显著低于正常宫颈组织(100.0%),P<0.05及P<0.01,但E-cadherin和nm 23-H 1阳性表达与宫颈癌的临床分期、组织学分级、间质浸润和淋巴结转移无关(P>0.05)。宫颈癌中CD 44v6表达与E-cadherin和nm 23-H 1表达呈负相关(P<0.01及P<0.05)。结论:在子宫颈癌中CD 44v6蛋白高表达和E-cadherin、nm 23-H 1蛋白低表达是判断宫颈癌的生物学行为的良好指标。     

MGMT启动子与垂体腺瘤侵略性行为及ADC值的相关性研究

目的 探讨垂体腺瘤O-6-甲基鸟嘌呤DNA甲基转移酶(MGMT)启动子甲基化状态与肿瘤侵略性行为及ADC值的相关性.方法 采用前瞻性研究,选取我院2019年01月至2020年08月收治的垂体腺瘤的患者,所有患者术前接受MRI检查(平扫+增强+解剖弥散),术后对肿瘤组织标本进行苏木精-伊红(HE)染色、免疫组化检查,通过...     

Wound,pressure ulcer and burn guidelines – 4: Guidelines for the management of connective tissue disease/vasculitis-associated skin ulcers

The Japanese Dermatological Association prepared guidelines focused on the treatment of skin ulcers associated with connective tissue disease/vasculitis practical in clinical settings of dermatological care. Skin ulcers associated with connective tissue diseases or vasculitis occur on the background of a wide variety of diseases including, typically, systemic sclerosis but also systemic lupus erythematosus (SLE), dermatomyositis, rheumatoid arthritis (RA), various vasculitides and antiphospholipid antibody syndrome (APS). Therefore, in preparing the present guidelines, we considered diagnostic/therapeutic approaches appropriate for each of these disorders to be necessary and developed algorithms and clinical questions for systemic sclerosis, SLE, dermatomyositis, RA, vasculitis and APS.