Predictors of infraspinatus muscle degeneration in individuals with an isolated supraspinatus tendon tear.

OBJECTIVE: Determine the demographic and clinical factors that predict infraspinatus muscle degeneration in individuals with an isolated supraspinatus tendon tear. MATERIALS AND METHODS: A retrospective analysis was performed using the medical records of patients who had a shoulder MRI interpreted by 1 of 3 fellowship-trained musculoskeletal radiologists since the implementation of a standardized MRI 3 T protocol within our healthcare system. Demographic (e.g., age, sex) and clinical data (e.g., tear size, muscle degeneration, co-morbidities) were collected. Patients with an isolated supraspinatus tendon tear (n = 121) were assigned to one of two groups based on whether any infraspinatus muscle degeneration was present. Logistic regression was used to assess the univariate relationships between infraspinatus muscle degeneration and patient and clinical data, while least absolute shrinkage and selector operator (LASSO) logistic regression was used to assess the multivariable relationship. RESULTS: Of the patients with an isolated supraspinatus tendon tear, 16.5% had evidence of infraspinatus muscle degeneration. The presence of infraspinatus muscle degeneration was independently associated with cardiovascular disease (P = 0.01), supraspinatus muscle degeneration (P < 0.01), and subscapularis muscle degeneration (P = 0.01). When the multivariable relationship is assessed, supraspinatus muscle degeneration emerged as the only variable of significant importance for detecting infraspinatus muscle degeneration (specificity: 87.1%, sensitivity: 80.0%). CONCLUSION: Infraspinatus muscle degeneration is not uncommon in individuals with an isolated supraspinatus tear and is most associated with concomitant supraspinatus muscle degeneration. These findings highlight the need for clinicians to specifically assess the status of each rotator cuff muscle, even when the tendon itself is intact.

Optimizing detection of postoperative leaks on upper gastrointestinal fluoroscopy: a step-by-step guide.

Postoperative leaks after gastrointestinal surgery are important to identify to decrease patient morbidity and mortality. Fluoroscopic studies are commonly employed to detect postoperative leak. While the literature addresses the sensitivity and specificity of these examinations, there is generally a lack of description of the fluoroscopic technique itself and there may be variability between radiologists in how these studies are performed. It is important to balance a standardized fluoroscopy protocol while tailoring the exam for each surgical and patient situation. Here we will briefly review common postoperative anatomy in the upper gastrointestinal tract, propose fluoroscopic techniques to improve postoperative leak detection, and illustrate teaching points with clinical cases.

Correlation of Baseline Visual Acuity with Outcomes of Treatment with Anti-VEGF in Neovascular Age-Related Macular Degeneration.

PURPOSE: Neovascular age-related macular degeneration (nv-AMD) is the leading cause of blindness in individuals 55 years and older. The advent of anti-vascular endothelial growth factor (anti-VEGF) therapy has greatly altered the visual acuity (VA) prognosis in these patients. While many studies have described treatment outcomes, few have explored the impact of early detection on VA outcomes. PATIENTS AND METHODS: This retrospective cohort study consisted of treatment-naïve eyes with nv-AMD (ICD9 diagnosis code 362.52) that were treated with bevacizumab, ranibizumab, and aflibercept by four physician investigators in a large urban tertiary center from March 2008 to October 2015. Eyes were categorized by baseline VA into good (20/50 or better), intermediate (20/50-20/200), and poor (20/200 or worse) initial VA. VA and optical coherence tomography (OCT) findings were evaluated throughout the treatment period. RESULTS: 224 eyes were evaluated. Of eyes with good, intermediate, and poor initial VA, 14.1%, 37.2%, and 58.3% showed an increase in 2 or more lines of vision on LogMAR, respectively [p < 0.001], while 71.8%, 40.7%, and 16.7% of eyes had a final VA of 20/50 or better, respectively [p < 0.001]. Average final Snellen VA in eyes with good, intermediate, and poor initial VA was 20/47, 20/96, and 20/277, respectively. Change in VA for good, intermediate, and poor initial VA groups was ΔLogMAR of +0.117, +0.041, and -0.230, respectively. Of eyes with good, intermediate, and poor baseline VA, 42.3%, 20.9%, and 20.0%, respectively, showed resolution of fluid on OCT [p = 0.003]. CONCLUSION: Patients with good initial VA were more likely to maintain good vision and show resolution of fluid on OCT through follow-up. Patients with poor initial VA tended to gain more vision, however, had poorer final VA. This underscores the importance of early detection and treatment of nv-AMD in maintaining superior outcomes.

Relationship between the dimerization of thyroglobulin and its ability to form triiodothyronine.

Thyroglobulin (TG) is the most abundant thyroid gland protein, a dimeric iodoglycoprotein (660 kDa). TG serves as the protein precursor in the synthesis of thyroid hormones tetraiodothyronine (T4) and triiodothyronine (T3). The primary site for T3 synthesis in TG involves an iodotyrosine acceptor at the antepenultimate Tyr residue (at the extreme carboxyl terminus of the protein). The carboxyl-terminal region of TG comprises a cholinesterase-like (ChEL) domain followed by a short unique tail sequence. Despite many studies, the monoiodotyrosine donor residue needed for the coupling reaction to create T3 at this evolutionarily conserved site remains unidentified. In this report, we have utilized a novel, convenient immunoblotting assay to detect T3 formation after protein iodination in vitro, enabling the study of T3 formation in recombinant TG secreted from thyrocytes or heterologous cells. With this assay, we confirm the antepenultimate residue of TG as a major T3-forming site, but also demonstrate that the side chain of this residue intimately interacts with the same residue in the apposed monomer of the TG dimer. T3 formation in TG, or the isolated carboxyl-terminal region, is inhibited by mutation of this antepenultimate residue, but we describe the first substitution mutation that actually increases T3 hormonogenesis by engineering a novel cysteine, 10 residues upstream of the antepenultimate residue, allowing for covalent association of the unique tail sequences, and that helps to bring residues Tyr2744 from apposed monomers into closer proximity.

De novo triiodothyronine formation from thyrocytes activated by thyroid-stimulating hormone.

The thyroid gland secretes primarily tetraiodothyronine (T4), and some triiodothyronine (T3). Under normal physiological circumstances, only one-fifth of circulating T3 is directly released by the thyroid, but in states of hyperactivation of thyroid-stimulating hormone receptors (TSHRs), patients develop a syndrome of relative T3 toxicosis. Thyroidal T4 production results from iodination of thyroglobulin (TG) at residues Tyr5 and Tyr130, whereas thyroidal T3 production may originate in several different ways. In this study, the data demonstrate that within the carboxyl-terminal portion of mouse TG, T3 is formed de novo independently of deiodination from T4 We found that upon iodination in vitro, de novo T3 formation in TG was decreased in mice lacking TSHRs. Conversely, de novo T3 that can be formed upon iodination of TG secreted from PCCL3 (rat thyrocyte) cells was augmented from cells previously exposed to increased TSH, a TSHR agonist, a cAMP analog, or a TSHR-stimulating antibody. We present data suggesting that TSH-stimulated TG phosphorylation contributes to enhanced de novo T3 formation. These effects were reversed within a few days after removal of the hyperstimulating conditions. Indeed, direct exposure of PCCL3 cells to human serum from two patients with Graves' disease, but not control sera, led to secretion of TG with an increased intrinsic ability to form T3 upon in vitro iodination. Furthermore, TG secreted from human thyrocyte cultures hyperstimulated with TSH also showed an increased intrinsic ability to form T3 Our data support the hypothesis that TG processing in the secretory pathway of TSHR-hyperstimulated thyrocytes alters the structure of the iodination substrate in a way that enhances de novo T3 formation, contributing to the relative T3 toxicosis of Graves' disease.