How Did the COVID-19 Pandemic Affect Trends in Facial Trauma?

Study Design: Retrospective cohort analysis. Objective: To examine the impact the COVID-19 pandemic and its accompanying societal measures had on the incidence, characteristics, and management of maxillofacial traumatic injuries. Methods: This cohort analysis compared facial trauma injuries presenting to the highest-volume Level I Trauma Center in New Jersey, USA from January 1 to July 31 in 2020 and 2019. Differences in demographics, mechanisms, and interventions were compared between the pandemic period (March 16-July 31, 2020) and the equivalent pre-pandemic date period in 2019 using X 2, Fishers Exact, and Mann-Whitney U testing. Results: In total, 616 subjects were included. The daily incidence of facial trauma consults during the 2020 pandemic (1.81 ± 1.1) decreased compared to 2019 (2.15 ± 1.3) (p = 0.042). During the outbreak, there was an increase in the proportion of subjects with positive urine drug screens (21.5% vs. 12.2%; p = 0.011) and injuries related to domestic violence (10.2% vs. 4.5%; p = 0.023). Patients were 30% less likely to be transferred from local hospitals (RR, 0.70 [0.53-0.93]; p = 0.014). Although subjects had a 25% increased risk of presenting with injuries deemed procedural (RR, 1.25 [95% CI, 1.05-1.56]; p = 0.048), a greater proportion were discharged with operative procedures scheduled as outpatients (16.0% vs. 4.9%; p = 0.005). Conclusions: The COVID-19 pandemic has impacted both the epidemiology and management of maxillofacial traumatic injuries, perhaps secondary to modifications in personal and community behaviors or the effects on healthcare systems in our region.

Deletion of phosphatidylserine flippase ß-subunit Tmem30a in satellite cells leads to delayed skeletal muscle regeneration.

Phosphatidylserine (PS) is distributed asymmetrically in the plasma membrane of eukaryotic cells. Phosphatidylserine flippase (P4-ATPase) transports PS from the outer leaflet of the lipid bilayer to the inner leaflet of the membrane to maintain PS asymmetry. The ß subunit TMEM30A is indispensable for transport and proper function of P4-ATPase. Previous studies have shown that the ATP11A and TMEM30A complex is the molecular switch for myotube formation. However, the role of Tmem30a in skeletal muscle regeneration remains elusive. In the current study, Tmem30a was highly expressed in the tibialis anterior (TA) muscles of dystrophin-null ( mdx) mice and BaCl 2-induced muscle injury model mice. We generated a satellite cell (SC)-specific Tmem30a conditional knockout (cKO) mouse model to investigate the role of Tmem30a in skeletal muscle regeneration. The regenerative ability of cKO mice was evaluated by analyzing the number and diameter of regenerated SCs after the TA muscles were injured by BaCl 2-injection. Compared to the control mice, the cKO mice showed decreased Pax7 + and MYH3 + SCs, indicating diminished SC proliferation, and decreased expression of muscular regulatory factors (MYOD and MYOG), suggesting impaired myoblast proliferation in skeletal muscle regeneration. Taken together, these results demonstrate the essential role of Tmem30a in skeletal muscle regeneration.

Management of goblet cell carcinoid.

BACKGROUND AND OBJECTIVES: Goblet cell carcinoid, a rare tumor of intermediate malignant potential, is known to account for a significant minority of appendiceal neoplasms. Sixteen new cases of gastrointestinal goblet cell carcinoid were reviewed to describe their presentation, treatment, and outcome. METHODS: A review of 16 cases from a single institution. RESULTS: Sixteen patients were diagnosed with goblet cell carcinoid between 1995 and 2005. Presenting diagnoses included appendicitis (n=8), abdominal or liver mass (n=5), uterine fibroids (n=1), ovarian mass (n=1), and Crohn's Disease exacerbation (n=1). Mean follow-up was 12 months with a mortality of 19% (n=3). Patients were divided into two groups: those where the diagnosis was an incidental finding at operation (Group 1) and those where the presentation was of an abdominal mass or metastatic disease (Group 2). Nine of ten patients in Group 1 initially received appendectomies. Group 2 included patients presenting with Krukenberg type lesions (n=2) and abdominal masses (n=4). CONCLUSIONS: Goblet cell carcinoid is a rare malignant tumor largely affecting the appendix. In patients presenting with appendicitis, our series does not support the recommendation of right hemicolectomy based on pathologic diagnosis alone and surgical intervention must be customized to the individual patient.

Ultraviolet light activates NFkappaB through translational inhibition of IkappaBalpha synthesis.

UV light induces a delayed and prolonged (3-20 h) activation of NFkappaB when compared with the immediate and acute (10-90 min) activation of NFkappaB in response to tumor necrosis factor alpha treatment. In the early phase (3-12 h) of NFkappaB activation, UV light reduces inhibitor of NFkappaB (IkappaB) through an IkappaB kinase-independent, but polyubiquitin-dependent, pathway. However, the mechanism for the UV light-induced reduction of IkappaB and activation of NFkappaB is not known. In this report, we show that UV light down-regulates the total amount of IkappaB through decreasing IkappaB mRNA translation. Our data show that UV light inhibits translation of IkappaB in wild-type mouse embryo fibroblasts (MEF(S/S)) and that this inhibition is prevented in MEF(A/A) cells in which the phosphorylation site, Ser-51 in the eukaryotic translation initiation factor 2 alpha-subunit, is replaced with a non-phosphorylatable Ala (S51A). Our data also show that UV light-induced NFkappaB activation is delayed in MEF(A/A) cells and in an MCF-7 cell line that is stably transfected with a trans-dominant negative mutant protein kinase-like endoplasmic reticulum kinase (PERK). These results suggest that UV light-induced eukaryotic translation initiation factor 2 alpha-subunit phosphorylation translationally inhibits new IkappaB synthesis. Without a continuous supply of newly synthesized IkappaB, the existing IkappaB is degraded through a polyubiquitin-dependent proteasomal pathway leading to NFkappaB activation. Based upon our results, we propose a novel mechanism by which UV light regulates early phase NFkappaB activation by means of an ER-stress-induced translational inhibition pathway.

Ultraviolet light inhibits translation through activation of the unfolded protein response kinase PERK in the lumen of the endoplasmic reticulum.

Exposure to ultraviolet light can cause inflammation, premature skin aging, and cancer. UV irradiation alters the expression of multiple genes that encode functions to repair DNA damage, arrest cell growth, and induce apoptosis. In addition, UV irradiation inhibits protein synthesis, although the mechanism is not known. In this report, we show that UV irradiation induces phosphorylation of eukaryotic translation initiation factor 2 on the alpha-subunit (eIF2alpha) and inhibits protein synthesis in a dosage- and time-dependent manner. The UV-induced phosphorylation of eIF2alpha was prevented by the overexpression of a non-phosphorylatable mutant of eIF2alpha (S51A). PERK is an eIF2alpha protein kinase localized to the endoplasmic reticulum that is activated by the accumulation of unfolded proteins in the endoplasmic reticulum. Expression of trans-dominant-negative mutants of PERK also prevented eIF2alpha phosphorylation upon UV treatment and protected from the associated translation attenuation. The luminal domain of dominant-negative mutant PERK formed heterodimers with endogenous PERK to inhibit the PERK signaling pathway. In contrast, eIF2alpha phosphorylation was not inhibited by overexpression of a trans-dominant-negative mutant kinase, PKR, supporting the theory that UV-induced eIF2alpha phosphorylation is specifically mediated by PERK. These results support a novel mechanism by which UV irradiation regulates translation via an endoplasmic reticulum-stress signaling pathway.