Traditional and novel imaging modalities for advanced prostate cancer: A critical review.

Accurate detection of metastatic prostate cancer in the setting of preoperative staging as well as posttreatment recurrence is crucial to provide patients with appropriate and timely treatment of their disease. This has traditionally been accomplished with a combination of computed tomography, magnetic resonance imaging, and bone scan. Recently, more novel imaging techniques have been developed to help improve the detection of advanced and metastatic prostate cancer. This review discusses the efficacy of the traditional imaging modalities as well as the novel imaging techniques in detecting metastatic prostate cancer. Articles discussed were gathered through a formal PubMed search.

Combination and Novel Pharmacologic Agents for OAB.

PURPOSE OF REVIEW: To evaluate recent literature on combination and novel pharmacologic therapies for overactive bladder (OAB). RECENT FINDINGS: Combination therapies demonstrating greater efficacy than monotherapy include combination anticholinergics, anticholinergic plus ß-3 agonist, and anticholinergic with behavioral modification, percutaneous tibial nerve stimulation, or sacral neuromodulation. Promising novel therapies include new bladder selective anticholinergics, new ß-3 agonists, and gabapentin. OAB is a symptom complex caused by dysfunction in the interconnected neural, muscular, and urothelial systems that control micturition. Although several therapeutic targets and treatment options exist, complete resolution is not always achieved, discontinuation rate for medical therapy is high, and few patients subsequently progress to third-line treatment options. Recent literature suggests combination therapy diversifying therapeutic targets is more effective than targeting a single pathway and novel treatments targeting additional pathways have promising results.

When do patients truly reach maximal medical improvement after undergoing reverse shoulder arthroplasty? The incidence and clinical significance of pain and patient-reported outcome measure improvement.

HYPOTHESIS: Patients receiving reverse total shoulder arthroplasty (RTSA) may reach MMI prior to 12 months postoperatively. BACKGROUND: With the growth of RTSA indications, there is a paucity of information regarding maximum medical improvement (MMI) after these procedures. Systems of evaluating recovery, such as patient-reported outcome measures and minimal clinically important differences (MCIDs) will allow for measurement of when patients reach maximum medical improvement (MMI) after these procedures. PURPOSE: To evaluate when patients have reached MMI after RTSA. METHODS: Patients were prospectively enrolled in the institution's RTSA registry. All patients undergoing RTSA who agreed to be enrolled were included. Patient-specific factors, American Shoulder and Elbow Surgeons Standardized Shoulder Assessment Form (ASES) score, and pain data were collected preoperatively and at 6 and 12 months postoperatively. Subgroup analysis was performed on preoperative diagnosis before analyzing MCID and MMI. MMI was calculated by using the last time point interval that an MCID did not occur. RESULTS: Of 182 patients, 92 had complete 12-month postoperative data, including visual analog scale (VAS) pain and ASES scores. Subgroup analysis showed preoperative diagnosis of rotator cuff arthropathy, revision surgery, glenohumeral arthritis, proximal humerus fracture, and chronic dislocation. All 5 groups had improvement that exceeded MCID thresholds at 6 months and variable improvement from 6-12 months. Analysis of variance compared the different groups, showing that VAS pain scores and ASES scores were different at all time points except for preoperative VAS pain scores. CONCLUSIONS: Patients undergoing RTSA may reach MMI at 6 months instead of the previously reported 1-year time point. Data from this study can allow providers to deliver value care and potentially limit visits after 6 months postoperatively.

Making Lemonade Together -- How Program Directors, Applicants, and Medical Schools Can Thrive During the Upcoming Interview Season.

This article was migrated. The article was marked as recommended. The virtual residency interview process ushers in a new era of medical education. Many stakeholders are increasingly concerned as validated recommendations regarding Match success appear less reliable, fossilized rules have become increasingly fluid, and traditional streams of communication have become inadequate. Program directors will look to sell their program using unvalidated methods. Applicants will make life-altering decisions using fewer data points than historically available. Medical schools will endeavor to advise their students as they gear up for breaking new ground. In this piece, we introduce considerations and recommendations for the main players involved in the virtual interview process. If each party prioritizes teamwork and communication, we can collectively tackle the challenges of the upcoming cycle and turn lemons into lemonade.

The Role of Chemoprophylactic Agents in Modulating Platelet Aggregability After Traumatic Brain Injury.

BACKGROUND: The pathophysiology behind the subacute but persistent hypercoagulable state after traumatic brain injury (TBI) is poorly understood but contributes to morbidity induced by venous thromboembolism. Because platelets and their microvesicles have been hypothesized to play a role in post-traumatic hypercoagulability, administration of commonly used agents may ameliorate this coagulability. We hypothesized that utilization of aspirin, ketorolac, amitriptyline, unfractionated heparin, or enoxaparin would modulate the platelet aggregation response after TBI. METHODS: Concussive TBI was induced by weight drop. Mice were then randomized to receive aspirin, ketorolac, amitriptyline, heparin, enoxaparin, or saline control at 2 and 8 h after TBI. Mice were sacrificed at 6 or 24 h after injury to determine coagulability by rotational thromboelastometry (ROTEM), platelet function testing with impedance aggregometry, and microvesicle enumeration. Platelet sphingolipid metabolites were analyzed by mass spectrometry. RESULTS: ROTEM demonstrated increased platelet contribution to maximum clot firmness at 6 h after TBI in mice that received aspirin or amitriptyline, but this did not persist at 24 h. By contrast, adenosine diphosphate- and arachidonic acid-induced platelet aggregation at 6 h was significantly lower in mice receiving ketorolac, aspirin, and amitriptyline compared with mice receiving saline at 6 h after injury and only arachidonic acid-initiated platelet aggregation was decreased by aspirin at 24 h. There were no differences in microvesicle production at either time point. Platelet sphingosine-1-phosphate levels were decreased at 6 h in the group receiving amitriptyline and increased at 24 h along with platelet ceramide levels at 24 h in the amitriptyline group. CONCLUSION: After TBI, amitriptyline decreased platelet aggregability and increased contribution to clot in a manner similar to aspirin. The amitriptyline effects on platelet function and sphingolipid metabolites may represent a possible role of the acid sphingomyelinase in the hypercoagulability observed after injury. In addition, inhibition of platelet reactivity may be an underappreciated benefit of low molecular weight heparins, such as enoxaparin.

UCH-L1 is a Poor Serum Biomarker of Murine Traumatic Brain Injury After Polytrauma.

BACKGROUND: Several serum biomarkers have been studied to diagnose incidence and severity of traumatic brain injury (TBI), but a reliable biomarker in TBI has yet to be identified. Ubiquitin carboxy-terminal hydrolase L1 (UCH-L1) has been proposed as a biomarker in clinical and preclinical studies, largely in the setting of isolated TBI or concussion. The aim of this study was to evaluate the performance of UCH-L1 as a serum biomarker in the setting of polytrauma and TBI. METHODS: Multiple variations of murine TBI and polytrauma models were used to evaluate serum biomarkers. The different models included TBI with and without hemorrhagic shock and resuscitation, isolated extremity vascular ligation, extremity ischemia/reperfusion, and blunt tail injury. Blood was drawn at intervals after injury, and serum levels of neuron-specific enolase, UCH-L1, creatine kinase, and syndecan-1 were evaluated by enzyme-linked immunosorbent assay. RESULTS: UCH-L1 levels were not significantly different between TBI, tail injury, and sham TBI. By contrast, neuron-specific enolase levels were increased in TBI mice compared with tail injury and sham TBI mice. UCH-L1 levels increased regardless of TBI status at 30 min and 4 h after hemorrhagic shock and resuscitation. In mice that underwent femoral artery cannulation followed by hemorrhagic shock/resuscitation, UCH-L1 levels were significantly elevated compared with shock sham mice at 4 h (3158 ± 2168 pg/mL, 4 h shock versus 0 ± 0 pg/mL, 4 h shock sham; P < 0.01) and at 24 h (3253 ± 2954 pg/mL, 24 h shock versus 324 ± 482 pg/mL, 24 h shock sham; P = 0.03). No differences were observed in UCH-L1 levels between the sham shock and the arterial ligation, vein ligation, or extremity ischemia/reperfusion groups at any time point. Similar to UCH-L1, creatine kinase was elevated only after shock compared with sham mice at 4, 24, and 72 h after injury. CONCLUSIONS: Our study demonstrates that UCH-L1 is not a specific marker for TBI but is elevated in models that induce central and peripheral nerve ischemia. Given the increase in UCH-L1 levels observed after hemorrhagic shock, we propose that UCH-L1 may be a useful adjunct in quantifying severity of shock or global ischemia rather than as a specific marker of TBI.