The degree of aortic occlusion in the setting of trauma alters the extent of acute kidney injury associated with mitochondrial preservation.

Resuscitative endovascular balloon occlusion of the aorta (REBOA) is used to control noncompressible hemorrhage not addressed with traditional tourniquets. However, REBOA is associated with acute kidney injury (AKI) and subsequent mortality in severely injured trauma patients. Here, we investigated how the degree of aortic occlusion altered the extent of AKI in a porcine model. Female Yorkshire-cross swine (n = 16, 68.1 ± 0.7 kg) were anesthetized and had carotid and bilateral femoral arteries accessed for REBOA insertion and distal and proximal blood pressure monitoring. Through a laparotomy, a 6-cm liver laceration was performed and balloon inflation was performed in zone 1 of the aorta for 90 min, during which animals were randomized to target distal mean arterial pressures of 25 or 45 mmHg via balloon volume adjustment. Blood draws were taken at baseline, end of occlusion, and time of death, at which point renal tissues were harvested 6 h after balloon deflation for histological and molecular analyses. Renal blood flow was lower in the 25-mmHg group (48.5 ± 18.3 mL/min) than in the 45-mmHg group (177.9 ± 27.2 mL/min) during the occlusion phase, which recovered and was not different after balloon deflation. AKI was more severe in the 25-mmHg group, as evidenced by circulating creatinine, blood urea nitrogen, and urinary neutrophil gelatinase-associated lipocalin. The 25-mmHg group had increased tubular necrosis, lower renal citrate synthase activity, increased tissue and circulating syndecan-1, and elevated systemic inflammatory cytokines. The extent of renal ischemia-induced AKI is associated with the magnitude of mitochondrial biomass and systemic inflammation, highlighting potential mechanistic targets to combine with partial REBOA strategies to prevent AKI.NEW & NOTEWORTHY Large animal models of ischemia-reperfusion acute kidney injury (IR-AKI) are lacking. This report establishes a titratable IR-AKI model in swine in which a balloon catheter can be used to alter distal pressures experienced by the kidney, thus controlling renal blood flow. Lower blood flow results in greater renal dysfunction and structural damage, as well as lower mitochondrial biomass, elevated systemic inflammation, and vascular dysfunction.

Functional traits of fossil plants.

A minuscule fraction of the Earth's paleobiological diversity is preserved in the geological record as fossils. What plant remnants have withstood taphonomic filtering, fragmentation, and alteration in their journey to become part of the fossil record provide unique information on how plants functioned in paleo-ecosystems through their traits. Plant traits are measurable morphological, anatomical, physiological, biochemical, or phenological characteristics that potentially affect their environment and fitness. Here, we review the rich literature of paleobotany, through the lens of contemporary trait-based ecology, to evaluate which well-established extant plant traits hold the greatest promise for application to fossils. In particular, we focus on fossil plant functional traits, those measurable properties of leaf, stem, reproductive, or whole plant fossils that offer insights into the functioning of the plant when alive. The limitations of a trait-based approach in paleobotany are considerable. However, in our critical assessment of over 30 extant traits we present an initial, semi-quantitative ranking of 26 paleo-functional traits based on taphonomic and methodological criteria on the potential of those traits to impact Earth system processes, and for that impact to be quantifiable. We demonstrate how valuable inferences on paleo-ecosystem processes (pollination biology, herbivory), past nutrient cycles, paleobiogeography, paleo-demography (life history), and Earth system history can be derived through the application of paleo-functional traits to fossil plants.

Cystocerebral Syndrome in a Patient with Altered Mental Status.

BACKGROUND Cystocerebral syndrome is delirium occurring in the elderly that results from urinary retention and acute bladder distension. Urinary retention can cause cerebral issues, such as altered mental status, without having an infection present. The pathophysiology is possibly due to increased catecholamine secretion while attempting to micturate. Due to its presenting symptoms, most physicians begin cerebrovascular workup, performing unnecessary and, often, invasive imaging studies. Although easily overlooked as a differential diagnosis, cystocerebral syndrome is an easily treatable cause of delirium and should be considered during treatment of elderly patients with delirium. CASE REPORT The patient was an 89-year-old man with a medical history of chronic obstructive airway disease, dementia, hypertensive disorder, and gastroesophageal reflux disease who presented with altered mental status secondary to urinary incontinence. The computed tomography scan without contrast showed a large volume of impacted stool in the cecum, with a distended urinary bladder. This case report describes his presentation, medical treatment, and outcome and discusses areas of gap improvement. CONCLUSIONS To date, there are only a handful of published articles on cystocerebral syndrome. This case report aims to add the awareness of bladder distention as an etiology of cystocerebral syndrome to the body of knowledge in the scientific community in the hope that patients will be identified and treated earlier, more safely, and at a reduced cost. Cystocerebral syndrome needs to be extensively addressed in research, and physicians should consider it one of the important differential diagnoses of delirium among elderly men.

Real-Time Measurements of Oral Mucosal Carbon Dioxide (POMCO2) Reveals an Inverse Correlation With Blood Pressure in a Porcine Model of Coagulopathic Junctional Hemorrhage.

INTRODUCTION: Shock states that occur during, for example, profound hemorrhage can cause global tissue hypoperfusion leading to organ failure. There is an unmet need for a reliable marker of tissue perfusion during hemorrhage that can be followed longitudinally. Herein, we investigated whether longitudinal POMCO2 tracks changes in hemodynamics in a swine model of coagulopathic uncontrolled junctional hemorrhage. MATERIALS AND METHODS: Female Yorkshire-crossbreed swine (n = 7, 68.1 ± 0.7 kg) were anesthetized and instrumented for continuous measurement of mean arterial pressure (MAP). Coagulopathy was induced by the exchange of 50 to 60% of blood volume with 6% Hetastarch over 30 minutes to target a hematocrit of <15%. A 4.5-mm arteriotomy was made in the right common femoral artery with 30 seconds of free bleeding. POMCO2 was continuously measured from baseline through hemodilution, hemorrhage, and a subsequent 3-h intensive care unit period. Rotational thromboelastometry and blood gases were measured. RESULTS: POMCO2 and MAP showed no significant changes during the hemodilution phase of the experiment, which produced coagulopathy evidenced by prolonged clot formation times. However, POMCO2 increased because of the uncontrolled hemorrhage by 11.3 ± 3.1 mmHg and was inversely correlated with the drop (17.9 ± 5.9 mmHg) in MAP (Y = -0.4122*X + 2.649, P = .02, r2 = 0.686). In contrast, lactate did not significantly correlate with the changes in MAP (P = .35) or POMCO2 (P = .37). CONCLUSIONS: Despite the logical appeal of measuring noninvasive tissue CO2 measurement as a surrogate for gastrointestinal perfusion, prior studies have only reported snapshots of this readout. The present investigation shows real-time longitudinal measurement of POMCO2 to confirm that MAP inversely correlates to POMCO2 in the face of coagulopathy. The simplicity of measuring POMCO2 in real time can provide an additional practical option for military or civilian medics to monitor trends in hypoperfusion during hemorrhagic shock.

Increased anxiety and emotional lability in a patient with SDHB gene mutation paraganglioma: a call to multidisciplinary approach.

Paragangliomas are neuroendocrine tumors that have the potential to secrete catecholamines. They have been linked to genetic mutations in the mitochondrial succinate dehydrogenase (SDH) complex. Patients can experience both physical symptoms and psychiatric symptoms like anxiety, depression, and psychosis. These symptoms can occur as paroxysmal episodes with periods of increased catecholamine secretion. We describe a patient with SDHB gene mutation, who has been diagnosed with a jugular paraganglioma, and was brought to the hospital under Baker Act for threats made online. Since diagnosis this patient has been experiencing both anxiety and post-traumatic stress disorder (PTSD). The patient and a family member report increased emotional lability, and the patient reports multiple daily episodes of anxiousness. This case outlines the connection between paragangliomas and psychiatric symptoms, the impact they can have on patients' daily lives, and the importance of addressing the possibility of these symptoms and establishing a multispecialty healthcare team at the time of diagnosis.

Are There More HER2 FISH in the Sea? An Institution's Experience in Identifying HER2 Positivity Using Fluorescent In Situ Hybridization in Patients with HER2 Negative Immunohistochemistry.

BACKGROUND: Approximately 20% of breast cancers express HER2-positive receptors in the USA. HER2 receptor immunohistochemistry (IHC) staining with equivocal (2+) results commonly undergoes fluorescence in-situ hybridization (FISH) for further classification. Current guidelines do not recommend routine FISH testing in IHC-negative (0 or 1+) cases. This study investigates an institution that performs both IHC and FISH testing on all cases to identify the true HER2-positive rate. PATIENTS AND METHODS: A retrospective chart review from 2015 to 2021 was conducted at an institution where both HER2 IHC and FISH testing were performed at the time of diagnosis for all invasive breast cancers. The rate of true HER2-positive patients was determined, and patient and tumor characteristics were further explored. RESULTS: A total of 1835 invasive breast cancer cases were primarily treated at this institution. A total of 289 cases were HER2 positive on IHC and FISH testing (15.7%). An additional 38 cases were identified as HER2 negative on IHC, but reclassified as HER2 positive on reflex FISH testing. Total HER2 positive cases increased from 289 (15.7%) to 327 cases (17.8%) with reflex FISH testing. CONCLUSIONS: The additional HER2-positive cases after completing FISH testing on IHC-negative tumors suggests there may be a role for routine FISH testing in addition to standard IHC staining to determine HER2 status for breast cancer. The ethical, prognostic and even  benefits of a correct diagnosis outweigh the added expense of FISH testing.

Providencia alcalifaciens in a patient with a staghorn calculus: a novel presentation.

A member of the Enterobacteriaceae family, Providencia alcalifaciens is typically recognized as a source of gastrointestinal illness. Although its pathogenicity is not well known, many studies have suggested its mechanism of action involves the invasion of the intestinal mucosal layer. Although P. alcalifaciens is a urease producing microorganism, it has not been associated with the formation of a staghorn calculus in the setting of a urinary tract infection. This organism is neither commonly pursued in research or investigation nor is it commonly tested for in the clinical setting. This is especially true when combined with other disease processes, such as calculus formation. The advancement of antibiotic resistance, such as carbapenemase-producing strains, should bring more attention and routine investigation to this organism in the acute stage of infection. In this case report we introduce a 43-year-old Cuban female, who presents with a left-sided staghorn calculi and urine culture positive for carbapenemase-producing P. alcalifaciens.

Evaluation of novel hemostatic agents in a coagulopathic swine model of junctional hemorrhage.

BACKGROUND: Hemostatic dressings are used extensively in both military and civilian trauma to control lethal noncompressible hemorrhage. The ideal topical hemostatic agent would provide reliable hemostasis in patients with profound acidosis, coagulopathy, and shock. This study aimed to compare next-generation hemostatic agents against the current military standard in a translational swine model of vascular injury and coagulopathy. METHODS: Female Yorkshire swine were randomized to eight groups (total n = 63; control n = 14, per group n = 7) of hemostatic agents and included: QuikClot Combat Gauze (Teleflex, Morrisville, NC), which served as the control; BloodSTOP IX (LifeScience Plus, Mountain View, CA); Celox Rapid (Medtrade Product, Crewe, United Kingdom); ChitoSAM 100 (Sam Medical, Tualatin, OR); EVARREST Fibrin Sealant Patch (Ethicon, Raritan, NJ); TAC Wrapping Gauze (H&H Medical, Williamsburg, VA); ChitoGauze XR Pro (Tricol Biomedical, Portland, OR); and X-Stat 30 (RevMedX, Wilsonville, OR). Hemodilution via exchange transfusion of 6% hetastarch was performed to induce acidosis and coagulopathy. An arteriotomy was created, allowing 30 seconds of free bleeding followed by application of the hemostatic agent and compression via an external compression device. A total of three applications were allowed for continued/recurrent bleeding. All blood loss was collected, and hemostatic agents were weighed to calculate blood volume loss. Following a 180-minute observation period, angiography was completed to evaluate for technical complication and distal perfusion of the limb. Finally, the limb was ranged five times to assess for rebleeding and clot stability. RESULTS: All swine were confirmed coagulopathic with rotational thromboelastography and acidotic (pH 7.2 ± 0.02). BloodSTOP IX allowed a significant increase in blood loss and number of applications required to obtain hemostasis compared with all other groups. BloodSTOP IX demonstrated a decreased survival rate (29%, p = 0.02). All mortalities were directly attributed to exsanguination as a result of device failure. In surviving animals, there was no difference in extravasation. BloodSTOP IX had an increased rebleeding rate after ranging compared with QuikClot Combat Gauze ( p = 0.007). CONCLUSION: Most novel hemostatic agents demonstrated comparable efficacy compared with the currently military standard hemostatic dressing, CG.

A Novel Sutureless Anastomotic Device in a Swine Model: A Proof of Concept Study.

INTRODUCTION: Vascular reconstruction requires technical expertise and is often time consuming. As a novel alternative to traditional hand-sewn vascular anastomoses, the VasoLock (VL), is a nonabsorbable, sutureless anastomosis device with traction anchors designed to hold free artery ends together. These anchors do not penetrate the vessel wall but adhere by leveraging the elasticity of the vessels to fasten blood vessels together. This pilot study assesses the performance and patency of this novel device in a porcine model of femoral artery injury. METHODS: Female swine (n = 7) underwent femoral artery exposure for a total of 10 VL implanted. Study animals underwent hemodilution to a target hematocrit of 15% and ROTEM was used to assess coagulopathy, followed by an arterial injury via transection. The VL was inserted without any sutures. Flow-probe monitors were positioned proximal and distal to the device and flow rates were measured continuously for a total of 90 min. Flow was analyzed and presented as a ratio of distal to proximal flow with the slope of this ratio across time subsequently determined. Angiographic assessment was completed to evaluate for patency and technical complications after 90 min of implant. RESULTS: The average animal weight was 44.1 ± 3.2 kg. The average mean arterial pressure at the time of implant was 51.2 ± 7.8 mmHg, median heart rate was 77.4 (IQR = 77.25-157.4) beats per minute, and average temperature was 36.1 ± 1.5°C. The baseline hematocrit was 13.5 ± 3.0%, average pH was 7.20 ± 0.1, average clotting time was 154.1 ± 58.7 s and average clot formation time was 103.4 ± 10.9 s all demonstrating the acidotic, hypothermic, and coagulopathic state of the swine at the time of insertion. During the 90-min observation period, the average flow gradient identified across the VL was 0.99 ± 0.24, indicating no significant change in flow across the VL. The average slope of the gradients was 0.0005 (P = 0.22), suggesting the ratio of proximal and distal flow did not change over the 90 min. Following 90 min of dwell time, all VL were patent without technical complication. Angiographic assessment at 90 min demonstrated no evidence of dissection, device migration, arterial extravasation, or thromboembolism with any of the 10 devices. CONCLUSIONS: This pilot study demonstrated technical feasibility of the novel VL device over a 90-min observation period. All VL were patent and no negative events or complications were identified. This technology demonstrated significant promise in a coagulopathic state: additional investigation, involving long-term survival, is warranted for further validation.

Exercise training remodels inguinal white adipose tissue through adaptations in innervation, vascularization, and the extracellular matrix.

Inguinal white adipose tissue (iWAT) is essential for the beneficial effects of exercise training on metabolic health. The underlying mechanisms for these effects are not fully understood, and here, we test the hypothesis that exercise training results in a more favorable iWAT structural phenotype. Using biochemical, imaging, and multi-omics analyses, we find that 11 days of wheel running in male mice causes profound iWAT remodeling including decreased extracellular matrix (ECM) deposition and increased vascularization and innervation. We identify adipose stem cells as one of the main contributors to training-induced ECM remodeling, show that the PRDM16 transcriptional complex is necessary for iWAT remodeling and beiging, and discover neuronal growth regulator 1 (NEGR1) as a link between PRDM16 and neuritogenesis. Moreover, we find that training causes a shift from hypertrophic to insulin-sensitive adipocyte subpopulations. Exercise training leads to remarkable adaptations to iWAT structure and cell-type composition that can confer beneficial changes in tissue metabolism.

Atypical Presentation of Gout: A Case Report.

Gout is the most common inflammatory arthritis which is caused by the buildup of uric acid crystals in the joints, that leads to severe pain, swelling, and stiffness. The condition typically affects the first metatarsophalangeal joint but it can impact other joints in the body. We present a case in which a 43-year-old male with a past medical history of obesity, hypertension, osteoarthritis, and gout presented with bilateral leg pain and the inability to walk for the last two years. Labs showed persistent leukocytosis, elevated ESR (erythrocyte sedimentation rate), normal uric acid levels, with physical exam findings of bilateral tender nodular leg lesions. Chest X-ray, head CT without contrast, left hip X-ray and ultrasound of left lower extremity were performed which were all negative. Biopsy of the tender skin nodules confirmed the diagnosis of tophaceous gout. Acute and prophylactic treatment of tophaceous gout resulted in resolved inflammation and leukocytosis without any complications.

Antagonistic effect of cyclin-dependent kinases and a calcium-dependent phosphatase on polyglutamine-expanded androgen receptor toxic gain of function.

Spinal and bulbar muscular atrophy is caused by polyglutamine (polyQ) expansions in androgen receptor (AR), generating gain-of-function toxicity that may involve phosphorylation. Using cellular and animal models, we investigated what kinases and phosphatases target polyQ-expanded AR, whether polyQ expansions modify AR phosphorylation, and how this contributes to neurodegeneration. Mass spectrometry showed that polyQ expansions preserve native phosphorylation and increase phosphorylation at conserved sites controlling AR stability and transactivation. In small-molecule screening, we identified that CDC25/CDK2 signaling could enhance AR phosphorylation, and the calcium-sensitive phosphatase calcineurin had opposite effects. Pharmacologic and genetic manipulation of these kinases and phosphatases modified polyQ-expanded AR function and toxicity in cells, flies, and mice. Ablation of CDK2 reduced AR phosphorylation in the brainstem and restored expression of Myc and other genes involved in DNA damage, senescence, and apoptosis, indicating that the cell cycle-regulated kinase plays more than a bystander role in SBMA-vulnerable postmitotic cells.

Use of MEDEVAC Resources in Austere Settings: Paget-Schroetter in the Deployed Environment.

Medical evacuation (MEDEVAC) from a combat zone requires complex decision-making and coordination of assets. A MEDEVAC helicopter team transports not only battle-injured patients but also patients with urgent non-battle-related medical diagnoses from extremely remote locations and are at the mercy of terrain, weather, and enemy contact. The military represents a young population particularly susceptible to venous thoracic outlet syndrome (vTOS) given the rigorous physical activity demands. Current literature supports immediate anticoagulation and surgical decompression within 14 days of diagnosis of vTOS to prevent long-term morbidity. Presented is a case of service member with vTOS presenting at an extremely remote military clinic who underwent a prompt evacuation ∼7,000 miles utilizing rotary-wing transport, followed by three to four more fixed-wing flights to a military treatment facility in the United States. Immediate recognition and ultrasound of this patient to confirm vTOS upon presentation and effective communication to non-medical military commanders and the receiving medical personnel at each Echelon was necessary to ensure an expedited evacuation. The surgeons treating this patient recommend prompt evacuation of deployed service members with suspected vTOS, venogram at the Role 3 if ultrasound is inconclusive, anticoagulation, and return to a Role 4 CONUS facility for definitive surgical management within 14 days. This case is an example of the efficiency of the military MEDEVAC system on a global scale, ensuring optimum medical care for all service members deployed.

What predicts suicidality among psychologists? An examination of risk and resilience.

Psychologists may have a uniquely high risk for suicide. We examined whether, among 172 psychologists, factors predicting suicide risk among the general population (e.g., gender and mental illness), occupational factors (e.g., burnout and secondary traumatic stress), and past trauma predicted suicidality. We also tested whether resilience and meaning in life were negatively related to suicidality and whether resilience buffered relationships between risk factors and suicidality. Family history of mental illness, number of traumas, and lifetime depression/anxiety predicted higher suicidality, whereas resilience predicted lower suicidality. At higher levels of resilience, the relationship between family history of suicide and suicidality was stronger.

Postoperative antiplatelet and/or anticoagulation use does not impact complication or reintervention rates after vein repair of arterial injury: A PROOVIT study.

INTRODUCTION: The use of antiplatelet (AP) and anticoagulation (AC) therapy after autogenous vein repair of traumatic arterial injury is controversial. The hypothesis in this study was that there is no difference in early postoperative outcomes regardless of whether AC, AP, both, or neither are used. METHODS: The American Association for the Surgery of Trauma (AAST) PROspective Observational Vascular Injury Treatment (PROOVIT) registry was queried from November, 2013, to January, 2019, for arterial injuries repaired with a vein graft. Demographics and injury characteristics were compared. Need for in-hospital reoperation was the primary outcome in this four-arm study, assessed with two ordinal logistic regression models (1. no therapy vs. AC only vs. AC and AP; 2. no therapy vs. AP only vs. AC and AP). RESULTS: 373 patients (52 no therapy, 88 AP only, 77 AC only, 156 both) from 19 centers with recorded Injury Severity Scores (ISS) were identified. Patients who received no therapy were younger than those who received AP (27.0 vs. 34.2, p = 0.02), had higher transfusion requirement (p < 0.01 between all groups) and a different distribution of anatomic injury (p < 0.01). After controlling for age, sex, ISS, platelet count, hemoglobin, pH, lactate, INR, transfusion requirement and anatomic location, there was no association with postoperative medical therapy and in-hospital operative reintervention, or any secondary outcome, including thrombosis (p = 0.67, p = 0.22). CONCLUSIONS: Neither AC nor AP alone, nor in combination, impact complication rate after arterial repair with autologous vein. These patients can be safely treated with or without antithrombotics, recognizing that this study did not demonstrate a beneficial effect.

HTT (huntingtin) and RAB7 co-migrate retrogradely on a signaling LAMP1-containing late endosome during axonal injury.

ABBREVIATIONS: Atg5: Autophagy-related 5; Atg8a: Autophagy-related 8a; AL: autolysosome; AP: autophagosome; BAF1: bafilomycin A1; BDNF: brain derived neurotrophic factor; BMP: bone morphogenetic protein; Cyt-c-p: Cytochrome c proximal; CQ: chloroquine; DCTN1: dynactin 1; Dhc: dynein heavy chain; EE: early endosome; DYNC1I1: dynein cytoplasmic 1 intermediate chain 1; HD: Huntington disease; HIP1/Hip1: huntingtin interacting protein 1; HTT/htt: huntingtin; iNeuron: iPSC-derived human neurons; IP: immunoprecipitation; Khc: kinesin heavy chain; KIF5C: kinesin family member 5C; LAMP1/Lamp1: lysosomal associated membrane protein 1; LE: late endosome; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MAP3K12/DLK: mitogen-activated protein kinase kinase kinase 12; MAPK8/JNK/bsk: mitogen-activated protein kinase 8/basket; MAPK8IP3/JIP3: mitogen-activated protein kinase 8 interacting protein 3; NGF: nerve growth factor; NMJ: neuromuscular junction; NTRK1/TRKA: neurotrophic receptor tyrosine kinase 1; NRTK2/TRKB: neurotrophic receptor tyrosine kinase 2; nuf: nuclear fallout; PG: phagophore; PtdIns3P: phosphatidylinositol-3-phosphate; puc: puckered; ref(2)P: refractory to sigma P; Rilpl: Rab interacting lysosomal protein like; Rip11: Rab11 interacting protein; RTN1: reticulon 1; syd: sunday driver; SYP: synaptophysin; SYT1/Syt1: synaptotagmin 1; STX17/Syx17: syntaxin 17; tkv: thickveins; VF: vesicle fraction; wit: wishful thinking; wnd: wallenda.

Acute worsening of CADASIL in a patient with COVID-19 infection: illustrative case.

BACKGROUND: Reports of cerebrovascular ischemia and stroke occurring as predominant neurological sequelae of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, which causes coronavirus disease 2019 (COVID-19), are increasingly evident within the literature. While various pathophysiological mechanisms have been postulated, including hypercoagulability, endothelial invasion, and systemic inflammation, discrete mechanisms for viral neurotropism remain unclear and controversial. OBSERVATIONS: The authors present a unique case study of a 64-year-old male with acute COVID-19 infection and acute worsening of previously stable cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a rare heritable arteriopathy due to mutation in the Notch3 gene, which is critical for vascular development and tone. Delayed cranial neuropathies, brainstem fluid-attenuated inversion recovery signal, and enhancement of olfactory and vagus nerves on magnetic resonance neurography in this patient further support viral neurotropism via cranial nerves in addition to cerebral vasculature. LESSONS: To the authors' knowledge, this is the first case in the literature that not only demonstrates the consequences of COVID-19 infection in a patient with altered cerebrovascular autoregulation such as CADASIL but also highlights the tropism of SARS-CoV-2 for (1) cranial nerves as a mode of entry to the central nervous system and (2) vessels as a cause of cerebrovascular ischemia.

Transmission visualizations of healthcare infection clusters: A scoping review.

Objective: To evaluate infectious pathogen transmission data visualizations in outbreak publications. Design: Scoping review. Methods: Medline was searched for outbreak investigations of infectious diseases within healthcare facilities that included ≥1 data visualization of transmission using data observable by an infection preventionist showing temporal and/or spatial relationships. Abstracted data included the nature of the cluster(s) (pathogen, scope of transmission, and individuals involved) and data visualization characteristics including visualization type, transmission elements, and software. Results: From 1,957 articles retrieved, we analyzed 30 articles including 37 data visualizations. The median cluster size was 20.5 individuals (range, 7-1,963) and lasted a median of 214 days (range, 12-5,204). Among the data visualization types, 10 (27%) were floor-plan transmission maps, 6 (16%) were timelines, 11 (30%) were transmission networks, 3 (8%) were Gantt charts, 4 (11%) were cluster map, and 4 (11%) were other types. In addition, 26 data visualizations (70%) contained spatial elements, 26 (70%) included person type, and 19 (51%) contained time elements. None of the data visualizations contained contagious periods and only 2 (5%) contained symptom-onset date. Conclusions: The data visualizations of healthcare-associated infectious disease outbreaks in the systematic review were diverse in type and visualization elements, though no data visualization contained all elements important to deriving hypotheses about transmission pathways. These findings aid in understanding the visualizing transmission pathways by describing essential elements of the data visualization and will inform the creation of a standardized mapping tool to aid in earlier initiation of interventions to prevent transmission.

A swine model of reproducible timed induction of peripheral arterial shunt failure: Developing warning signs of imminent shunt failure.

Temporary intravascular shunts are used to maintain perfusion in injured vessels, although failure can be unpredictable and lead to significant morbidity. The aim of the present study was to develop a dose- and timing-controlled swine model of intrinsic shunt failure to facilitate the development of a warning system for impending failure. Ten Yorkshire swine (weight, 56.6 ± 4.2 kg) underwent bilateral Argyle shunt (Cardinal Health, Dublin, OH) placement in the external iliac arteries, with proximal cannulation of the circumflex iliac arteries for infusion of thrombin. The thrombin infusion was randomized to the left or right side for 5000 vs 10,000 U/h. The 5000-U/h group required 2.1 times as long as the 10,000-U/h group to reach failure (mean, 21.8 minutes vs 46.4 minutes; P < .0001), as shown by a Kaplan-Meier survival analysis (log-rank P < .0001). However, the 5000-U/h group required the same total amount of thrombin (mean, 3752 ± 856 U; P = .57). Thus, time- and/or thrombin dose-controlled induction of shunt failure is technically feasible. Furthermore, in the final 15 minutes before failure, the flow was similar between the two groups (P > .05), and the slope of the flow curve became more negative the closer the model was to failure. Overall, this model could be used to develop an alert system to predict for impending shunt failure or the need for intervention.