다중혈관 관상동맥 환자에서 y-문합을 이용하여 양쪽 내흉동맥만을 사용한 우회술의 조기 성적

世界経済・社会統計 = World development indicators

Acute kidney injury (AKI) is a complex disorder for which currently there is no accepted definition. Having a uniform standard for diagnosing and classifying AKI would enhance our ability to manage these patients. Future clinical and translational research in AKI will require collaborative networks of investigators drawn from various disciplines, dissemination of information via multidisciplinary joint conferences and publications, and improved translation of knowledge from pre-clinical research. We describe an initiative to develop uniform standards for defining and classifying AKI and to establish a forum for multidisciplinary interaction to improve care for patients with or at risk for AKI. Members representing key societies in critical care and nephrology along with additional experts in adult and pediatric AKI participated in a two day conference in Amsterdam, The Netherlands, in September 2005 and were assigned to one of three workgroups. Each group's discussions formed the basis for draft recommendations that were later refined and improved during discussion with the larger group. Dissenting opinions were also noted. The final draft recommendations were circulated to all participants and subsequently agreed upon as the consensus recommendations for this report. Participating societies endorsed the recommendations and agreed to help disseminate the results. The term AKI is proposed to represent the entire spectrum of acute renal failure. Diagnostic criteria for AKI are proposed based on acute alterations in serum creatinine or urine output. A staging system for AKI which reflects quantitative changes in serum creatinine and urine output has been developed. We describe the formation of a multidisciplinary collaborative network focused on AKI. We have proposed uniform standards for diagnosing and classifying AKI which will need to be validated in future studies. The Acute Kidney Injury Network offers a mechanism for proceeding with efforts to improve patient outcomes.

Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury

Summary Background Since December, 2019, Wuhan, China, has experienced an outbreak of coronavirus disease 2019 (COVID-19), caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Epidemiological and clinical characteristics of patients with COVID-19 have been reported but risk factors for mortality and a detailed clinical course of illness, including viral shedding, have not been well described. Methods In this retrospective, multicentre cohort study, we included all adult inpatients (≥18 years old) with laboratory-confirmed COVID-19 from Jinyintan Hospital and Wuhan Pulmonary Hospital (Wuhan, China) who had been discharged or had died by Jan 31, 2020. Demographic, clinical, treatment, and laboratory data, including serial samples for viral RNA detection, were extracted from electronic medical records and compared between survivors and non-survivors. We used univariable and multivariable logistic regression methods to explore the risk factors associated with in-hospital death. Findings 191 patients (135 from Jinyintan Hospital and 56 from Wuhan Pulmonary Hospital) were included in this study, of whom 137 were discharged and 54 died in hospital. 91 (48%) patients had a comorbidity, with hypertension being the most common (58 [30%] patients), followed by diabetes (36 [19%] patients) and coronary heart disease (15 [8%] patients). Multivariable regression showed increasing odds of in-hospital death associated with older age (odds ratio 1·10, 95% CI 1·03–1·17, per year increase; p=0·0043), higher Sequential Organ Failure Assessment (SOFA) score (5·65, 2·61–12·23; p Interpretation The potential risk factors of older age, high SOFA score, and d-dimer greater than 1 μg/mL could help clinicians to identify patients with poor prognosis at an early stage. Prolonged viral shedding provides the rationale for a strategy of isolation of infected patients and optimal antiviral interventions in the future. Funding Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences; National Science Grant for Distinguished Young Scholars; National Key Research and Development Program of China; The Beijing Science and Technology Project; and Major Projects of National Science and Technology on New Drug Creation and Development.

Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study

http://hub.hku.hk/bitstream/10722/235686/1/content.pdf

Worldwide trends in diabetes since 1980: a pooled analysis of 751 population-based studies with 4.4 million participants

Performance Simulation of an Integrated Organic Rankine Cycle and Air Inter-Cooling System for Heavy-Duty Diesel Truck Engines

OBJECTIVE To explore the involvement of metabotropic glutamate receptors (mGluRs) in the formation of cerebral edema. METHODS Male Wistar rats weighing from 250 g to 300 g were used. Trans-1-aminocyclopentane-1, 3-diacarboxylic acid (tACPD), an agonist of mGluRs, was microinjected into the right caudatum. Brain water content was determined by a wet weight/dry weight technique and Na+, K+ and Ca2+ contents were measured by inductive Couple Plasma-9000 at 6 h, 24 h and 48 h post-injection. Extravasation of Evan's blue (EB) into the brain was determined as an indicator of disturbance in the blood-brain barrier (BBB) and endothelial cells. Histologic studies were performed under a Leitz microscope and a Philips EM208s electron microscope. RESULTS Dose-dependent and time-related increase of brain water was induced after tACPD (10, 50, 500 and 1000 nmol) injection. A significant increase in Na+ and K+ content but not in Ca2+ content was observed. EB extravasation showed no blue stain, indicating no increase in BBB permeability induced by tACPD-injection. Electron microscope study confirmed this finding and revealed remarkable swelling of astrocytes especially endfoot processes of astrocytes around capillaries at 6 h after tACPD-injection. In addition, all changes mentioned above occurred in both caudatum. CONCLUSION These results indicate that activation of mGluRs by tACPD injected into the caudatum induced cytotoxic brain edema and interfered with astrocyte K+ buffering. This may provide new clues for therapeutic intervention.

Development of cytotoxic cerebral edema in rats following intracaudatum injection of tACPD, an agonist of metabotropic glutamate receptors.

The invention provides a reinforcement wire wound inner concave beam frame. Sections of an upper beam 1 and a lower beam 2 are all in inversely concave shapes; an inner margin of the beam comprises a base plane 6 and two transition arc surfaces 5; an outer margin 4 of the beam and an inner margin arc 5 are positioned on the same side of the diameter 7 of an outer margin arc of the beam. The inner concave beam of the frame has simple structure, is easy to be processed and assembled, effectively utilizes space, reduces the overall height of the frame, improves the overall stability and lightens the weight. The inner margin structure of the beam, which is determined suitable, can ensure that the beam has relatively small tensile stress under any state, thereby improving the fatigue strength of the beam, being a comparatively ideal beam structure frame with controllable low tensile stress and having wide application prospect.

Reinforcement wire wound inner concave beam frame

Silk sericin-based biomaterials shine in food and pharmaceutical industries

Background The delayed repair process in the aging diabetic population is becoming an alarming public health concern. ICAM-1 plays an important role in orchestrating the repair process by mediating neutrophil recruitment and phagocytosis. However, little is known about the role of ICAM-1 in aging diabetic repair. Methods By causing injury in aging diabetic mice with ICAM-1 deletion (AD-ICAM-1−/−), we found that AD-ICAM-1−/− mice exhibited a delayed repair process with incomplete re-epithelialization and reduced angiogenesis. Additionally, high-throughput Illumina sequencing was performed to evaluate the microbiota of such mice. Results The results indicate that the microbiota of the AD-ICAM-1−/− injury site differed taxonomically at both the phylum and genus levels. Neutrophil recruitment and phagocytic function were also reduced in the AD-ICAM-1−/− group. Notably, major inflammatory biomarker expression was also detected in AD-ICAM-1−/− injured tissue. Conclusions Overall, this study demonstrated that AD-ICAM-1−/− mice exhibit delayed repair. In addition, neutrophil recruitment and phagocytic activity were impaired in the AD-ICAM-1−/− group, which may have allowed microbes to colonize the injury site.

Lei Zhang

Papers

Performance Simulation of an Integrated Organic Rankine Cycle and Air Inter-Cooling System for Heavy-Duty Diesel Truck Engines

Development of cytotoxic cerebral edema in rats following intracaudatum injection of tACPD, an agonist of metabotropic glutamate receptors.

Reinforcement wire wound inner concave beam frame

Silk sericin-based biomaterials shine in food and pharmaceutical industries

ICAM-1 deletion delays the repair process in aging diabetic mice.