Adoption and Implementation of Intensive Planting Systems for Apple - The New Zealand Experience

Stuart D. Tustin,John Palmer 한국원예학회 2006 한국원예학회 기타간행물 Vol.- No.-

Does Percutaneous Lumbosacral Pedicle Screw Instrumentation Prevent Long-Term Adjacent Segment Disease after Lumbar Fusion?

Changoor Stuart,Faloon Michael Joseph,Dunn Conor John,Sahai Nikhil,Issa Kimona,Sinha Kumar,Hwang Ki Soo,Emami Arash 대한척추외과학회 2021 Asian Spine Journal Vol.15 No.3

Study Design: Retrospective cohort study. Purpose: To assess long-term clinical outcomes of adjacent segment disease (ASD) in patients who underwent lumbar interbody fusion with percutaneous pedicle screw (PS) instrumentation. Overview of Literature: ASD is a well-known sequela of spinal fusion, and is reported to occur at a rate of 2%–3% per year. There is debate as to whether ASD is a result of the instrumentation and fusion method or is the natural history of the patient’s disease. Minimally invasive percutaneous PS augmentation of lumbar interbody fusion aims to prevent the disruption of posterior soft tissue stabilizers. Methods: From 2004–2014, 419 consecutive patients underwent anterior, lateral, or minimally invasive transforaminal lumbar interbody fusion with percutaneous PS placement at a single institution. The mean follow-up was 4.5 years. The primary outcome measure was reoperation due to ASD. Patients were divided into two cohorts: those who underwent revision surgery secondary to ASD and those who did not require further surgery. Radiographic parameters were performed using postoperative radiographs. Patients with a pelvic incidence–lumbar lordosis (PI–LL) mismatch >10° were noted. Results: Revision proportion secondary to ASD was 4.77% (n=20). Mean time to revision surgery was 2.5 years. Revision rate secondary to ASD was 1.1% per year. Patients who developed ASD were younger than those who did not (50.5 vs. 56.9 years, p=0.015). There was no difference in number of levels fused between cohorts. Revision proportion secondary to ASD was similar between approaches (anterior, lateral, minimally invasive). There was no significant difference in PI–LL mismatch between those who underwent revision for ASD and those who did not (22.2% vs. 18.8%, p=0.758). Conclusions: ASD rates in patients who underwent percutaneous PS placement were lower than those previously published after open PS placement, possibly related to greater preservation of the posterior stabilizing elements of the lumbar spine.

Collagen-Induced Arthritis and the Potential Role of Autoimmunity to Type 2 Collagen in Rheumatoid Arthritis

Xiao Wen He,John M. Stuart,Linda K. Myers,Andrew H. Kang 대한류마티스학회 2002 대한류마티스학회지 Vol.9 No.1

Collagen induced arthritis (CIA) is an animal model that in many ways resembles rheumatoid arthritis (RA). CIA can be induced in susceptible animals by immunization with type II collagen (CII). Like RA, CIA is characterized by intense joint inflammation and destruction. On histological examination, there is synovitis accompanied by erosion of cartilage and subchondral bone. Autoantibodies to CII initiate joint inflammation by binding to articular cartilage, forming antigen-antibody complexes locally and activating hemolytic complement. Susceptibility to CIA in mice is linked to the expression of specific class II MHC molecules, which dictate the T cell determinants on CII, and therefore, the subsets of T cells that can be activated by CII. In addition to activation of B cells reactive to CII, the T cells stimulate monocytes/macrophages. These cells amplify the inflammatory cascade by secretion of proinflammatory monokines, including TNF-α and IL-1, leading to the production of other proinflammatory proteins, including matrix metalloproteinases (MMPs). The importance of CIA lies in its possible relationship to arthritis in humans. Progress in understanding CIA has contributed to the development of new therapies for RA. In addition, it has been found that mice with human HLA-DR1, DR4 and HLA-DQ8 transgenes, which have been demonstrated to be the susceptibility markers for RA, confer susceptibility to CIA. These observations coupled with the finding of T cells and B cells reactive with CII in the inflamed joints of RA patients establish the potential role of CII autoimmunity in the pathogenesis of RA.

Determinants of Variability in ISG15 Gene Expression in Patients with Chronic Hepatitis B (CHB) Infection during Treatment with Oral TLR7 Agonist GS-9620

Yoon Jun Kim,Stuart Gordon,Shyamasundaran Kottili,BenedettaMassetto,Anuj Gaggar,Scott Stem,Stefan Pflanz,Zhishen Ye,Mani Subramanian,John McHutchison,Young-Suk Lim,Ed Gane 한국간담췌외과학회 2014 한국간담췌외과학회 학술대회지 Vol.2014 No.4

Reciprocal Control of the Circadian Clock and Cellular Redox State - a Critical Appraisal

Putker, Marrit,O'Neill, John Stuart Korean Society for Molecular and Cellular Biology 2016 Molecules and cells Vol.39 No.1

Redox signalling comprises the biology of molecular signal transduction mediated by reactive oxygen (or nitrogen) species. By specific and reversible oxidation of redoxsensitive cysteines, many biological processes sense and respond to signals from the intracellular redox environment. Redox signals are therefore important regulators of cellular homeostasis. Recently, it has become apparent that the cellular redox state oscillates in vivo and in vitro, with a period of about one day (circadian). Circadian timekeeping allows cells and organisms to adapt their biology to resonate with the 24-hour cycle of day/night. The importance of this innate biological timekeeping is illustrated by the association of clock disruption with the early onset of several diseases (e.g. type II diabetes, stroke and several forms of cancer). Circadian regulation of cellular redox balance suggests potentially two distinct roles for redox signalling in relation to the cellular clock: one where it is regulated by the clock, and one where it regulates the clock. Here, we introduce the concepts of redox signalling and cellular timekeeping, and then critically appraise the evidence for the reciprocal regulation between cellular redox state and the circadian clock. We conclude there is a substantial body of evidence supporting circadian regulation of cellular redox state, but that it would be premature to conclude that the converse is also true. We therefore propose some approaches that might yield more insight into redox control of cellular timekeeping.

Is aggressive intravenous fluid prescription the answer to reduce mortality in severe pancreatitis? The FLIP study: Fluid resuscitation in pancreatitis

Julia McGovern,Samuel J Tingle,Northern Surgical Trainees Research Association (NOSTRA),Stuart Robinson,John Moir 한국간담췌외과학회 2023 Annals of hepato-biliary-pancreatic surgery Vol.27 No.4

Backgrounds/Aims: Acute pancreatitis is an emergency presentation, which can range from mild to life threatening. Intravenous fluids are the cornerstone of management. Although the WATERFALL trial described the optimal fluid rate in mild/moderate pancreatitis, this trial excluded patients with moderate-severe/severe pancreatitis. The aim of this study was to establish clinical practice regarding intravenous fluid administration in acute pancreatitis and assess its effect on mortality. Methods: Prospective multi-centre audit of patients with acute pancreatitis was conducted. Data were collected regarding intravenous fluid administration within 72 hours of admission. The primary outcome was 30-day mortality. Multivariable logistic regression was used to identify predictors of 30-day mortality. Results: Those with severe pancreatitis received more fluid; median 5.7 L versus 4 L in 72 hours (p = 0.003). Participants with severe pancreatitis who died within 30 days received a median of 2,750 mL in the first 24 hours, compared to 4,000 mL in those who survived. The following factors were significant predictors of 30-day mortality: age, Glasgow score, C-reactive protein, ischaemic heart disease, and pancreatitis aetiology. Overall, volume of intravenous fluid was not associated with mortality. However, the effect of intravenous fluid volume on mortality differed significantly depending on pancreatitis severity. In severe pancreatitis, increased volume of intravenous fluid was associated with significant reductions in mortality (odds ratio = 0.655; 0.459–0.936; p = 0.020). Conclusions: In severe pancreatitis, more aggressive fluid prescription was associated with decreased mortality; however, this was not the case in milder disease. Further prospective trials guiding fluid resuscitation in severe pancreatitis are needed, as the impact of fluid on this population appears to differ from that in those with milder disease.

Original Article : Rescue Endoscopic Ultrasound (EUS)-Guided Trucut Biopsy Following Suboptimal EUS-Guided Fine Needle Aspiration for Mediastinal Lesions

( Min Cho Chang ),( Mohammad Al Haddad ),( Julia K. Leblanc ),( Stuart Sherman ),( Mchenry Lee ),( John Dewitt ) 대한간학회 2013 Gut and Liver Vol.7 No.2

Background/Aims: Endoscopic ultrasound-guided fine needle aspiration (EUS-FNA) and Trucut biopsy (TCB) are sensitive techniques for diagnosing mediastinal lesions, but it is unclear how either one or both should be used to obtain a pathologic diagnosis. The objective of our study was to evaluate whether EUS-TCB impacts the diagnosis of mediastinal lesions after the initial on-site review of EUS-FNA specimen suggests a suboptimal result. Methods: We enrolled consecutive patients with mediastinal lesions who underwent EUS-TCB during the same procedure if the initial EUS-FNA demonstrated an inadequate FNA sample or suggested that histopathology was required for diagnosis. Diagnostic accuracies between procedures were compared as the main outcome. Results: Twenty-seven patients (14 men; median age, 56 years; range, 19 to 82 years) underwent EUS-FNA and EUS-TCB to evaluate a mediastinal lymphadenopathy or mass (n=17), to determine the cancer stage (n=3) or to exclude tumor recurrence or metastasis (n=7). The overall diagnostic accuracies of EUS-FNA and EUS-TCB were 78% and 67%, respectively (p=0.375). The combined diagnostic accuracy of EUS-FNA plus EUS-TCB was 82%. In six patients with nondiagnostic EUS-FNA, EUS-TCB provided a final diagnosis in one patient (17%). Conclusions: In the current series of patients with mediastinal masses or adenopathy, the administration of EUS-TCB following suboptimal results for the on-site cytology review did not increase the diagnostic yield. (Gut Liver 2013;7:150-156)

Association of Spinal Alignment Correction With Patient-Reported Outcomes in Adult Cervical Deformity: Review of the Literature

Elie Massaad,Muhamed Hadzipasic,Ali Kiapour,Asad M. Lak,Ganesh Shankar,Hasan A. Zaidi,Stuart H. Hershman,John H. Shin 대한척추신경외과학회 2021 Neurospine Vol.18 No.3

Objective: Adult cervical deformity (ACD) is a debilitating spinal condition that causes significant pain, neurologic dysfunction, and functional impairment. Surgery is often performed to correct cervical alignment, but the optimal amount of correction required to improve patient-reported outcomes (PROs) are not yet well-defined. Methods: A review of the literature was performed and Fisher z-transformation (Zr) was used to pool the correlation coefficients between alignment parameters and PROs. The strength of correlation was defined according to the following: poor (0<r≤0.3), fair (0.3<r≤0.5), moderate (0.5<r≤0.8), and strong (0.8<r≤1). Results: Increased C2–7 sagittal vertical axis was fairly associated with increased Neck Disability Index (NDI) (pooled Zr=0.31; 95% confidence interval [CI], -0.03 to 0.58). Changes in T1 slope minus cervical lordosis poorly correlated with NDI (pooled Zr=-0.04; 95% CI, -0.23 to 0.30). Increased C7–S1 was poorly associated with worse EuroQoL 5-Dimension (pooled Zr=-0.22; 95% CI, -0.36 to -0.06). Correction of horizontal gaze did not correlate with legacy metrics. Modified Japanese Orthopedic Association correlated with C2-slope, C7–S1, and C2–S1. Conclusion: Spinal alignment parameters variably correlated with improved health-related quality of life and myelopathy after corrective surgery for ACD. Further studies evaluating legacy PROs, Patient-Reported Outcomes Measurement System, and ACD specific instruments are needed for further validation.

Identification of IRF8, TMEM39A, and IKZF3-ZPBP2 as Susceptibility Loci for Systemic Lupus Erythematosus in a Large-Scale Multiracial Replication Study

Marta E. Alarcon-Riquelme for the BIOLUPUS and GENLES Networks,Lessard, Christopher J.,Adrianto, I.,Ice, John A.,Wiley, Graham B.,Kelly, Jennifer A.,Glenn, Stuart B.,Adler, Adam J.,Li, H.,Rasmussen, A University of Chicago Press [etc.] 2012 American journal of human genetics Vol.90 No.4

Systemic lupus erythematosus (SLE) is a chronic heterogeneous autoimmune disorder characterized by the loss of tolerance to self-antigens and dysregulated interferon responses. The etiology of SLE is complex, involving both heritable and environmental factors. Candidate-gene studies and genome-wide association (GWA) scans have been successful in identifying new loci that contribute to disease susceptibility; however, much of the heritable risk has yet to be identified. In this study, we sought to replicate 1,580 variants showing suggestive association with SLE in a previously published GWA scan of European Americans; we tested a multiethnic population consisting of 7,998 SLE cases and 7,492 controls of European, African American, Asian, Hispanic, Gullah, and Amerindian ancestry to find association with the disease. Several genes relevant to immunological pathways showed association with SLE. Three loci exceeded the genome-wide significance threshold: interferon regulatory factor 8 (IRF8; rs11644034; p<SUB>meta-Euro</SUB> = 2.08 x 10<SUP>-10</SUP>), transmembrane protein 39A (TMEM39A; rs1132200; p<SUB>meta-all</SUB> = 8.62 x 10<SUP>-9</SUP>), and 17q21 (rs1453560; p<SUB>meta-all</SUB> = 3.48 x 10<SUP>-10</SUP>) between IKAROS family of zinc finger 3 (AIOLOS; IKZF3) and zona pellucida binding protein 2 (ZPBP2). Fine mapping, resequencing, imputation, and haplotype analysis of IRF8 indicated that three independent effects tagged by rs8046526, rs450443, and rs4843869, respectively, were required for risk in individuals of European ancestry. Eleven additional replicated effects (5 x 10<SUP>-8</SUP> < p<SUB>meta-Euro</SUB> < 9.99 x 10<SUP>-5</SUP>) were observed with CFHR1, CADM2, LOC730109/IL12A, LPP, LOC63920, SLU7, ADAMTSL1, C10orf64, OR8D4, FAM19A2, and STXBP6. The results of this study increase the number of confirmed SLE risk loci and identify others warranting further investigation.

Variation of sexual dimorphism and asymmetry in disease expression of inflammatory arthritis among laboratory mouse models with different genomic backgrounds

Wei Dong,Cheng Tian,Z. Galvin Li,David Brand,Yanhong Cao,Xiaoyun Liu,Jiamin Ma,Andy Chai,LindaK.myers,Jian Yan,Karen Hasty,John Stuart,Yan Jiao,Weikuan Gu,Xiaojun Cai 한국실험동물학회 2023 Laboratory Animal Research Vol.39 No.4

Sex difference has shown in the arthritis diseases in human population and animal models. We investigate how the sex and symmetry vary among mouse models with different genomic backgrounds. Disease data of sex and limbs accumulated in the past more than two decades from four unique populations of murine arthritis models were analyzed. They are (1) interleukin-1 receptor antagonist (IL-1ra) deficient mice under Balb/c background (Balb/c KO); (2) Mice with collagen II induced arthritis under DBA/1 background; (3) Mice with collagen II induced arthritis under C57BL/6 (B6) background and (4) A F2 generation population created by Balb/c KO X DBA/1 KO. Our data shows that there is a great variation in sexual dimorphism for arthritis incidence and severity of arthritis in mice harboring specific genetic modifications. For a F2 population, the incidence of arthritis was 57.1% in female mice and 75.6% in male mice. There was a difference in severity related to sex in two populations: B6.DR1/ B6.DR4 (P < 0.001) and F2 (P = 0.023) There was no difference Balb/c parental strain or in collagen-induced arthritis (CIA) in DBA/1 mice. Among these populations, the right hindlimbs are significantly higher than the scores for the left hindlimbs in males (P < 0.05). However, when examining disease expression using the collagen induced arthritis model with DBA/1 mice, sex-dimorphism did not reach statistical significance, while left hindlimbs showed a tendency toward greater disease expression over the right. Sexual dimorphism in disease expression in mouse models is strain and genomic background dependent. It sets an alarm that potential variation in sexual dimorphism among different racial and ethnic groups in human populations may exist. It is important to not only include both sexes and but also pay attention to possible variations caused by disease expression and response to treatment in all the studies of arthritis in animal models and human populations.