Tumor-associated macrophages trigger MAIT cell dysfunction at the HCC invasive margin.

Mucosal-associated invariant T (MAIT) cells represent an abundant innate-like T cell subtype in the human liver. MAIT cells are assigned crucial roles in regulating immunity and inflammation, yet their role in liver cancer remains elusive. Here, we present a MAIT cell-centered profiling of hepatocellular carcinoma (HCC) using scRNA-seq, flow cytometry, and co-detection by indexing (CODEX) imaging of paired patient samples. These analyses highlight the heterogeneity and dysfunctionality of MAIT cells in HCC and their defective capacity to infiltrate liver tumors. Machine-learning tools were used to dissect the spatial cellular interaction network within the MAIT cell neighborhood. Co-localization in the adjacent liver and interaction between niche-occupying CSF1R+PD-L1+ tumor-associated macrophages (TAMs) and MAIT cells was identified as a key regulatory element of MAIT cell dysfunction. Perturbation of this cell-cell interaction in ex vivo co-culture studies using patient samples and murine models reinvigorated MAIT cell cytotoxicity. These studies suggest that aPD-1/aPD-L1 therapies target MAIT cells in HCC patients.

Structural, Spectroscopic, and Computational Analysis of Heterometallic Thorium Phosphinidiide Complexes.

To synthesize complexes with thorium-phosphorus multiple-bond character, reactions of (C5Me5)2Th[P(H)Mes]2 with monovalent alkali-metal bases, MN(SiMe3)2, as well as CuMes, have been investigated. The results with MN(SiMe3)2 are phosphinidiide complexes of the form {(C5Me5)2Th[µ2-P(Mes)][µ2-P(H)Mes]M(L)n}2 (M = Na, n = 0; M = K, L = THF, n = 1; M = Rb, L = THF, n = 1; M = Cs, L = Et2O, n = 1). With CuMes, the product is a Th2Cu3P5 heterometallic structure, {(C5Me5)2Th[(µ2-P(H)Mes)P(Mes)]Cu}2Cu[µ2-P(H)Mes]. All complexes have been characterized using heteronuclear NMR and IR spectroscopy, density functional theory calculations, and their solid-state structure identified by X-ray crystallography. We also report the structure of {(C5Me5)2Th[(µ2-As(H)Mes)As(Mes)]Cu}2Cu[µ2-As(H)Mes] obtained from (C5Me5)2Th[As(H)Mes]2 with CuMes.

Growth Factor Signaling Regulates Mechanical Nociception in Flies and Vertebrates.

Mechanical sensitization is one of the most difficult clinical pain problems to treat. However, the molecular and genetic bases of mechanical nociception are unclear. Here we develop a Drosophila model of mechanical nociception to investigate the ion channels and signaling pathways that regulate mechanical nociception. We fabricated von Frey filaments that span the subthreshold to high noxious range for Drosophila larvae. Using these, we discovered that pressure (force/area), rather than force per se, is the main determinant of aversive rolling responses to noxious mechanical stimuli. We demonstrated that the RTK PDGF/VEGF receptor (Pvr) and its ligands (Pvfs 2 and 3) are required for mechanical nociception and normal dendritic branching. Pvr is expressed and functions in class IV sensory neurons, whereas Pvf2 and Pvf3 are produced by multiple tissues. Constitutive overexpression of Pvr and its ligands or inducible overexpression of Pvr led to mechanical hypersensitivity that could be partially separated from morphological effects. Genetic analyses revealed that the Piezo and Pain ion channels are required for mechanical hypersensitivity observed upon ectopic activation of Pvr signaling. PDGF, but not VEGF, peptides caused mechanical hypersensitivity in rats. Pharmacological inhibition of VEGF receptor Type 2 (VEGFR-2) signaling attenuated mechanical nociception in rats, suggesting a conserved role for PDGF and VEGFR-2 signaling in regulating mechanical nociception. VEGFR-2 inhibition also attenuated morphine analgesic tolerance in rats. Our results reveal that a conserved RTK signaling pathway regulates baseline mechanical nociception in flies and rats.SIGNIFICANCE STATEMENT Hypersensitivity to touch is poorly understood and extremely difficult to treat. Using a refined Drosophila model of mechanical nociception, we discovered a conserved VEGF-related receptor tyrosine kinase signaling pathway that regulates mechanical nociception in flies. Importantly, pharmacological inhibition of VEGF receptor Type 2 signaling in rats causes analgesia and blocks opioid tolerance. We have thus established a robust, genetically tractable system for the rapid identification and functional analysis of conserved genes underlying mechanical pain sensitivity.

Non-accidental harms ('abuse') in athletes with impairment ('para athletes'): a state-of-the-art review.

OBJECTIVE: Para athletes reap significant health benefits from sport but are vulnerable to non-accidental harms. Little is known about the types and impacts of non-accidental harms Para athletes face. In this literature review, we summarise current knowledge and suggest priorities for future research related to non-accidental harms in Para athletes. DESIGN: Six electronic databases were searched between August and September 2017. 2245 articles were identified in the initial title/abstract review, and 202 records were selected for full-text review following preliminary screening. Two independent examiners evaluated each full text, and eight citations were selected based on inclusion/exclusion criteria. DATA SOURCES: MEDLINE, Embase, PsycInfo, Cumulative Index to Nursing and Allied Health Literature, Scopus and Academic Search Premier. ELIGIBILITY CRITERIA FOR SELECTING STUDIES: Inclusion criteria: (A) human participants; (B) written in English; (C) descriptive, cohort and case series, case-control, qualitative, mixed methods studies and all clinical trials; and (D) data pertain to harassment/abuse of youth, recreational, collegiate, national-level and/or elite-level athletes with a physical and/or intellectual impairment. RESULTS: Most studies focused on young, visually impaired athletes and approximately half of all studies described high rates of bullying and its social implications. One study confirmed remarkably high rates of psychological, physical and sexual harms in Para athletes, compared with able-bodied peers. CONCLUSIONS: Bullying in young, visually impaired athletes is described most commonly in the available literature. Due to the limited amount of data, the prevalence of non-accidental harms in Para athletes remains unclear and information on trends over time is similarly unavailable.

Prostate epithelial cell of origin determines cancer differentiation state in an organoid transformation assay.

The cell of origin for prostate cancer remains a subject of debate. Genetically engineered mouse models have demonstrated that both basal and luminal cells can serve as cells of origin for prostate cancer. Using a human prostate regeneration and transformation assay, our group previously demonstrated that basal cells can serve as efficient targets for transformation. Recently, a subpopulation of multipotent human luminal cells defined by CD26 expression that retains progenitor activity in a defined organoid culture was identified. We transduced primary human prostate basal and luminal cells with lentiviruses expressing c-Myc and activated AKT1 (myristoylated AKT1 or myrAKT1) to mimic theMYCamplification andPTENloss commonly detected in human prostate cancer. These cells were propagated in organoid culture before being transplanted into immunodeficient mice. We found that c-Myc/myrAKT1-transduced luminal xenografts exhibited histological features of well-differentiated acinar adenocarcinoma, with strong androgen receptor (AR) and prostate-specific antigen (PSA) expression. In contrast, c-Myc/myrAKT1-transduced basal xenografts were histologically more aggressive, with a loss of acinar structures and low/absent AR and PSA expression. Our findings imply that distinct subtypes of prostate cancer may arise from luminal and basal epithelial cell types subjected to the same oncogenic insults. This study provides a platform for the functional evaluation of oncogenes in basal and luminal epithelial populations of the human prostate. Tumors derived in this fashion with defined genetics can be used in the preclinical development of targeted therapeutics.

Metal-Ligand Multiple Bonding in Thorium Phosphorus and Thorium Arsenic Complexes.

The complexes (C5 Me5 )2 Th(EHTipp)2 , (E=P or As; Tipp=2,4,6-triisopropylphenyl), provide a ligand framework that results in facile access to rare Th-E multiple bonds. The reaction of (C5 Me5 )2 Th(EHTipp)2 with KN(SiMe3 )2 , proceeds cleanly to the desired bridging phosphinidiide or arsinidiide complex, [{(C5 Me5 )2 Th(µ2 -ETipp)(µ2 -EHTipp)}K]2 under ambient conditions. In the absence of a chelating agent, the potassium cation of one monomeric unit interacts with the aryl ring of a second monomer to form a bridged dimer. In the presence of 2,2,2-cryptand, the terminal phosphinidene complex, [(C5 Me5 )2 Th=PTipp(PHTipp)][K(2,2,2-cryptand)] is isolated. Using X-ray crystallographic analysis, we have determined these complexes display the shortest Th-P and Th-As bond lengths reported.

The Gut Microbiome Controls Liver Tumors via the Vagus Nerve.

Liver cancer ranks amongst the deadliest cancers. Nerves have emerged as an understudied regulator of tumor progression. The parasympathetic vagus nerve influences systemic immunity via acetylcholine (ACh). Whether cholinergic neuroimmune interactions influence hepatocellular carcinoma (HCC) remains uncertain. Liver denervation via hepatic vagotomy (HV) significantly reduced liver tumor burden, while pharmacological enhancement of parasympathetic tone promoted tumor growth. Cholinergic disruption in Rag1KO mice revealed that cholinergic regulation requires adaptive immunity. Further scRNA-seq and in vitro studies indicated that vagal ACh dampens CD8+ T cell activity via muscarinic ACh receptor (AChR) CHRM3. Depletion of CD8+ T cells abrogated HV outcomes and selective deletion of Chrm3 on CD8 + T cells inhibited liver tumor growth. Beyond tumor-specific outcomes, vagotomy improved cancer-associated fatigue and anxiety-like behavior. As microbiota transplantation from HCC donors was sufficient to impair behavior, we investigated putative microbiota-neuroimmune crosstalk. Tumor, rather than vagotomy, robustly altered fecal bacterial composition, increasing Desulfovibrionales and Clostridial taxa. Strikingly, in tumor-free mice, vagotomy permitted HCC-associated microbiota to activate hepatic CD8+ T cells. These findings reveal that gut bacteria influence behavior and liver anti-tumor immunity via a dynamic and pharmaceutically targetable, vagus-liver axis.

Dislocated Extensor Mechanism in a Child With Bilateral Absent Patella Without Other Congenital Abnormalities.

CASE: A 10-year-old boy presented with bilateral absent patella and dislocation of the extensor mechanism in the left lower extremity. He underwent a lateral release and medial plication of the extensor mechanism with a Roux-Goldthwait procedure, followed by casting and bracing treatment. The patient fully recovered with a return to sports and improved active range of motion. CONCLUSION: Bilateral absent patella without other congenital anomalies is an exceedingly rare condition and can be accompanied by a dislocation of the extensor mechanism. Treatment should address functional limitations, including extensor mechanism dislocation, when present.

Cooperative dihydrogen activation with unsupported uranium-metal bonds and characterization of a terminal U(iv) hydride.

Cooperative chemistry between two or more metal centres can show enhanced reactivity compared to the monometallic fragments. Given the paucity of actinide-metal bonds, especially those with group 13, we targeted uranium(iii)-aluminum(i) and -gallium(i) complexes as we envisioned the low-valent oxidation state of both metals would lead to novel, cooperative reactivity. Herein, we report the molecular structure of [(C5Me5)2(MesO)U-E(C5Me5)], E = Al, Ga, Mes = 2,4,6-Me3C6H2, and their reactivity with dihydrogen. The reaction of H2 with the U(iii)-Al(i) complex affords a trihydroaluminate complex, [(C5Me5)2(MesO)U(µ2-(H)3)-Al(C5Me5)] through a formal three-electron metal-based reduction, with concomitant formation of a terminal U(iv) hydride, [(C5Me5)2(MesO)U(H)]. Noteworthy is that neither U(iii) complexes nor [(C5Me5)Al]4 are capable of reducing dihydrogen on their own. To make the terminal hydride in higher yields, the reaction of [(C5Me5)2(MesO)U(THF)] with half an equivalent of diethylzinc generates [(C5Me5)2(MesO)U(CH2CH3)] or treatment of [(C5Me5)2U(i)(Me)] with KOMes forms [(C5Me5)2(MesO)U(CH3)], which followed by hydrogenation with either complex cleanly affords [(C5Me5)2(MesO)U(H)]. All complexes have been characterized by spectroscopic and structural methods and are rare examples of cooperative chemistry in f element chemistry, dihydrogen activation, and stable, terminal ethyl and hydride compounds with an f element.

VIP interneurons in sensory cortex encode sensory and action signals but not direct reward signals.

Vasoactive intestinal peptide (VIP) interneurons in sensory cortex modulate sensory responses based on global exploratory behavior and arousal state, but their function during non-exploratory, goal-directed behavior is not well understood. In particular, whether VIP cells are activated by sensory cues, reward-seeking actions, or directly by reinforcement is unclear. We trained mice on a Go/NoGo whisker touch detection task that included a delay period and other features designed to separate sensory-evoked, action-related, and reward-related neural activity. Mice had to lick in response to a whisker stimulus to receive a variable-sized reward. Using two-photon calcium imaging, we measured ΔF/F responses of L2/3 VIP neurons in whisker somatosensory cortex (S1) during behavior. In both expert and novice mice, VIP cells were strongly activated by whisker stimuli and goal-directed actions (licking), but not by reinforcement. VIP cells showed somatotopic whisker tuning that was spatially organized relative to anatomical columns in S1, unlike lick-related signals which were spatially widespread. In expert mice, lick-related VIP responses were suppressed, not enhanced, when a reward was delivered, and the amount of suppression increased with reward size. This reward-related suppression was not seen in novice mice, where reward delivery was not yoked to licking. These results indicate that besides arousal and global state variables, VIP cells are activated by local sensory features and goal-directed actions, but not directly by reinforcement. Instead, our results are consistent with a role for VIP cells in encoding the expectation of reward associated with motor actions.

A seasonal idiopathic hepatitis syndrome in horses presented to a Midwestern veterinary teaching hospital.

OBJECTIVE: To report history, clinical examination findings, clinicopathologic findings, diagnostic test results, treatment, and outcome in horses with a novel idiopathic hepatitis syndrome. ANIMALS: 13 client-owned horses. PROCEDURES: Medical records of horses that were presented with fever and increased blood liver enzyme activity over a 16-month period were reviewed (December 1, 2020, to April 1, 2022). Collected data included signalment, history, clinical and clinicopathologic findings, diagnostic test results, treatment, clinical progression, and short-term outcome. RESULTS: Affected horses were presented between December and April of each of the 2 seasons investigated. The majority of horses developed cyclic fevers over the course of 3 weeks, during which time histologic evidence of hepatitis was observed. Histologic lesions included hepatic necrosis, neutrophilic to lymphohistiocytic inflammation, biliary epithelial injury, and portal fibrosis. Systemic inflammation was evidenced by increased serum amyloid A concentration and leukon changes. No horse developed signs of hepatic insufficiency, and all horses clinically recovered. Return of serum activity of GGT to within the reference range occurred within 16 weeks in most horses. Histologic lesions remained evident up to 27 weeks after initial presentation in 1 horse. CLINICAL RELEVANCE: Although an etiologic agent has not been identified, an apparently seasonal equine hepatitis syndrome was characterized by fever, systemic inflammation, increased liver enzyme activity, and histologic evidence of hepatitis. An infectious cause is suspected on the basis of histology and outcome.

Increased Neurovascular Morbidity Is Seen in Documented Knee Dislocation Versus Multiligamentous Knee Injury.

UPDATE: This article was updated on May 19, 2021 because of previous errors, which were discovered after the preliminary version of the article was posted online. In the legend for Figure 3-A, the phrase that had read "T1-weighted coronal MRI showing a right knee" now reads "T1-weighted coronal MRI showing a left knee." On page 924, in the section entitled "Materials and Methods," the sentence that had read "If there was no radiographic evidence or if there was a clinical note that documented visible deformity around the knee with no reduction maneuver being performed, then the patient was classified into the non-dislocated MLKI group." now reads "If there was no radiographic evidence or if there was no clinical note that documented visible deformity around the knee with no reduction maneuver being performed, then the patient was classified into the non-dislocated MLKI group." On page 925, in the section entitled "Analysis," the sentence that had read "Our study included 78 dislocated MLKIs and non-dislocated MLKIs, so both cohorts were adequately powered for the overall analysis." now reads "Our study included 45 dislocated MLKIs and 78 non-dislocated MLKIs, so both cohorts were adequately powered for the overall analysis." Finally, on page 927, in the section entitled "Discussion," the sentence that had read "Interestingly, we found that MLKIs with a documented knee dislocation had a substantially higher rate of vascular injury (23%) compared with those without (3%)." now reads "Interestingly, we found that MLKIs with a documented knee dislocation had a substantially higher rate of vascular injury (18%) compared with those without (4%)."

The terms "knee dislocation" and "multiligamentous knee injury" (MLKI) have been used interchangeably in the literature, and MLKI without a documented knee dislocation has often been described as a knee dislocation that "spontaneously reduced." We hypothesized that MLKI with documented tibiofemoral dislocation represents a more severe injury than MLKI without documented dislocation. We aimed to better characterize the injuries associated with documented knee dislocations versus MLKIs without evidence of tibiofemoral dislocation. A total of 124 patients who were treated for an MLKI or knee dislocation to a single level-I trauma center between January 2001 and January 2020 were retrospectively reviewed. Patients were stratified into 2 groups, those with and those without a documented knee dislocation, and 123 of 124 patients were included in the analysis (78 in the non-dislocated group and 45 in the dislocated group). Data regarding patient demographics, injury pattern, and associated neurovascular injury were collected and compared between groups. Dislocated MLKIs, compared with non-dislocated MLKIs, had higher rates of peroneal nerve injury (38% versus 14%, respectively; p = 0.004), vascular injury (18% versus 4%; p = 0.018), and an increased number of medial-sided injuries (53% versus 30%; p = 0.009). There was no difference between dislocated and non-dislocated MLKIs in the number of bicruciate ligament injuries (82% versus 77%, respectively; p = 0.448), or lateral-sided injuries (73% versus 74%; p = 0.901). Dislocated MLKIs were found to have increased rates of neurovascular injury compared with non-dislocated MLKIs, suggesting that knee dislocation and MLKI may not be synonymous in terms of associated injuries. Not all MLKIs are the result of a knee dislocation, and thus a documented tibiofemoral dislocation is a distinct entity that carries a greater risk of neurovascular compromise. We propose that these terms not be used interchangeably as previously described, and also that a high degree of vigilance must be maintained to evaluate for potential limb-threatening neurovascular injuries in any type of MLKI. Prognostic Level III . See Instructions for Authors for a complete description of levels of evidence.

Negative Pressure Incisional Therapy and Postoperative Infection after Posterior Approach Primary Total Hip Arthroplasty.

A major complication after total hip arthroplasty (THA) is infection, which can have devastating clinical and financial results. Silver-impregnated dry dressings, such as Aquacel dressings, and incisional negative pressure dressings (Prevena) have been developed to reduce the rates of surgical site infections (SSIs) after surgery. We retrospectively reviewed the medical records of 235 patients who underwent primary posterior approach THA at our institution during a three-year period. Patients were grouped based on surgical dressing. Rates of SSI were recorded, as well as the effects of factors including age, sex, body mass index, and medical comorbidities. In the high-risk subgroup, defined as BMI > 30 and ASA > 3, the infection rate was 2.97% in the Aquacel group, compared to 1.20% in the Prevena group. This difference did not reach statistical significance. There was a statistically significant impact on readmissions rate (p = 0.028) and reoperation (p = 0.001). The findings of this study suggest that negative pressure dressings in carefully selected patients may help to reduce reoperations and readmissions in this subgroup.

The Surgical Anatomy and the Deep Plane Thread Lift of the Buccal Fat Pad.

BACKGROUND: Management of facial rejuvenation by the thread lift procedure has evolved over the past few years. The role of deep plane thread lift for buccal fat pad reposition was advocated. However, there are concerns about the risks and the feasibility of the deep plane thread lift. This study was designed to determine whether the deep plane thread lift could achieve effective aesthetic results and to investigate the possible risks of critical tissue injury through cadaveric studies. METHODS: Twelve fresh frozen cephalic specimens of 8 male and 4 female Asian body donors (mean age, 63.3 ± 8.0 years) were investigated. The deep plane thread lifts for reposition of the buccal fat pads were performed for all the left hemifaces. Cadaveric dissections were performed to investigate the moving distance of the buccal fat pad and to examine the surrounding tissue of the passage of the deep plane thread lift. RESULTS: The average moving distance of the buccal fat pads after the deep plane thread lift was 3.73 cm. The difference in moving distance of buccal fat pads between bilateral sides was statistically significant (P < 0.001). No injuries of the critical vessels or nerves were found after cadaveric dissection. The passage of the deep plane thread lift was evaluated. CONCLUSION: The deep plane thread lift for reposition of the buccal fat pad is a safe, effective, and practical method.

The Pathoanatomy of Posterolateral Corner Ligamentous Disruption in Multiligament Knee Injuries Is Predictive of Peroneal Nerve Injury.

BACKGROUND: A description of the precise locations of ligamentous and myotendinous injury patterns of acute posterolateral corner (PLC) injuries and their associated osseous and neurovascular injuries is lacking in the literature. PURPOSE: To characterize the ligamentous and myotendinous injury patterns and zones of injury that occur in acute PLC injuries and determine associated rates of peroneal nerve palsies and vascular injuries, as well as fracture and dislocation. STUDY DESIGN: Case series; Level of evidence, 4. METHODS: We retrospectively identified all patients treated for an acute multiligament knee injury (MLKI) at our level 1 trauma center from 2001 to 2018. From this cohort, all patients with PLC injuries were identified. Demographics, involved ligaments and tendons, neurovascular injury, and presence of fracture and dislocation were compared with the larger multiligament knee cohort. Incidence and location of injury of PLC structures-from proximal to midsubstance and distal injury-were recorded. RESULTS: A total of 100 knees in 100 patients were identified as having MLKIs. A total of 74 patients (74%) had lateral-sided ligament injuries. Of these, 23 (31%) had a peroneal nerve palsy associated with their injury; 10 (14%), a vascular injury; and 23 (31%), a fracture. Patients with PLC injuries had higher rates of peroneal nerve injury as compared with those having acute MLKIs without a PLC injury (31% vs 4%; P = .005). Patients with a complete peroneal nerve palsy (n = 17) were less likely to regain function than those with a partial peroneal nerve palsy (n = 6; 12% vs 100%; P < .0001). Complete injury to the lateral collateral ligament (LCL) occurred in 71 of 74 (96%) PLC injuries, with 3 distinct patterns of injury demonstrated. Fibular avulsion of the LCL was the most common zone of injury (65%), followed by femoral avulsion (20%) and midsubstance tear (15%). Location of injury to the LCL was associated with the rate of peroneal nerve injury, with midsubstance tears and fibular avulsions associated with higher rates of peroneal nerve injury. CONCLUSION: MLKIs with involvement of the PLC are more likely to suffer peroneal nerve injury. The LCL is nearly always involved, and its location of injury is predictive of peroneal nerve injury. Patients with a complete peroneal nerve palsy at presentation are much less likely to regain function.

Mixed odontogenic tumors in four young dogs: ameloblastic fibroma and ameloblastic fibro-odontoma.

Ameloblastic fibroma (AF) and ameloblastic fibro-odontoma (AFO) are mixed odontogenic tumors (odontogenic tumors with induction) that are reported only rarely in dogs. These tumors are histologically complex and, to a degree, recapitulate the early stages of tooth development, comprising 2 types of tissue: neoplastic odontogenic epithelium, and induced ectomesenchyme (dental pulp). AFOs are distinguished from AFs by the additional presence of hard dental matrices such as dentin. Herein, we describe the key diagnostic features of AF and AFO in 4 young dogs.

Negative Pressure Incisional Therapy and Infection After Direct Anterior Approach Primary Total Hip Arthroplasty.

With the aging of the US population, total hip arthroplasty (THA) is becoming an increasingly common procedure. A major concern after THA is reducing infection rates, as infections can cause devastating complications. Improved sterile technique, standardized infection control protocols, and novel dressings have been used to reduce postoperative surgical site infections (SSIs). The use of either silver-impregnated dry dressings or easily applied incisional negative pressure dressings is aimed at reducing the rates of SSIs after primary anterior THA. The authors retrospectively reviewed the medical records of 275 patients who underwent anterior THA at their institution during a 1-year period. Patients were separated into groups based on their surgical dressing. Rates of SSI were documented, and the effects of various factors, including age, sex, body mass index, and comorbidities, were compared between the 2 cohorts. The authors also analyzed high-risk patients to determine whether easily applied incisional negative pressure dressings reduced infections. The use of easily applied incisional negative pressure dressings after primary anterior THA did not have a statistically significant impact on SSI rate (P=.42). There was also no difference in SSI, readmission, or reoperation in the high-risk group. The goal of using an incisional negative pressure wound therapy device is to help further decrease the risk of SSI. This study's findings suggest that the SSI rate in this group did not differ from that in the standard dressing group, such that the prophylactic use of a negative pressure wound therapy device is not indicated for either standard or high-risk patients undergoing primary anterior approach THA. [Orthopedics. 2019; 42(6):e539-e544.].