Ετικέτες

Πέμπτη 22 Απριλίου 2021

Reconstructive Management of Gunshot Wounds to the Frontal Sinus: An Urban Trauma Center's Perspective

xlomafota13 shared this article with you from Inoreader

Ann Plast Surg. 2021 Apr 21. doi: 10.1097/SAP.0000000000002857. Online ahead of print.

ABSTRACT

INTRODUCTION: In the last decade, we have seen a steady increase in the incidence of frontal sinus trauma due to gunshot wounds and a decrease in motor vehicle trauma. Penetrating gunshot wounds to the frontal sinus present a unique challenge to the reconstructive surgeon because they require careful consideration of the management principles of plastic surgery. Despite previous reviews on frontal sinus trauma, there are no studies examining the management techniques of frontal sinus fractures due specifically to gunshot wounds. In this study, we aim to retrospectively evaluate the use of a variety of tissue flaps in intervention and associated outcomes.

METHODS: A retrospective chart review was completed on all patients with gunshot wound(s) to the frontal sinus from January 2010 to January 2018 at a single institution. The patients were cla ssified based on the fracture pattern (anterior vs posterior table vs both), degree of displacement, presence of nasofrontal outflow tract injury, and evidence of cerebrospinal fluid leak. Patients were then stratified according to the type of reconstruction performed (cranialization, obliteration and need for free flap) and evaluated for major and minor complications after reconstruction.

RESULTS: In this study, we present outcome data from 28 cases of frontal sinus trauma due to gunshot wounds. There was a statistically significant difference (P = 0.049) in the type reconstructive strategy employed with each type of flap, with pericranial flaps primarily used in cranialization, temporal grafts were more likely to be used in obliteration, and free flaps were more likely to be used in cranialization. The overall major complication rate was 52% (P = 0.248), with the most common acute major complication was cerebrospinal fluid leak (39%) and major chronic was abscess (23.5%).

CONCLUSIONS: This report explores the management of frontal sinus trauma and presents short-term outcomes of treatment for penetrating gunshot wounds at a tertiary referral center.

PMID:33883442 | DOI:10.1097/SAP.0000000000002857

View on the web

Methylomic analysis identifies C11orf87 as a novel epigenetic biomarker for GI cancers

xlomafota13 shared this article with you from Inoreader

by Mita T. M. T. Tran, Kun-Tu Yeh, Yu-Ming Chuang, Po-Yen Hsu, Jie-Ting Low, Himani Kumari, Yu-Ting Lee, Yin-Chen Chen, Wan-Hong Huang, Hongchuan Jin, Shu-Hui Lin, Michael W. Y. Chan

Gastric cancer is one of the leading causes of cancer death worldwide. Previous studies demonstrated that activation of STAT3 is crucial for the development and progression of gastric cancer. However, the role of STAT3 in neuronal related gene methylation in gastric cancer has never been explored. In this study, by using DNA methylation microarray, we identified a potential STAT3 target, C11orf87, showing promoter hypomethylation in gastric cancer patients with lower STAT3 activation and AGS gastric cancer cell lines depleted with STAT3 activation. Although C11orf87 methylation is independent of its expression, ectopic expression of a constitutive activated STAT3 mutant upregulated its expression in gastric cancer cell line. Further bisulfite pyrosequencing demonstrated a progressive increase in DNA methylation of this target in patient tissues from gastritis, intestinal metaplasia, to gastric cancer. Intriguingly, patients with higher C11orf87 methylation was as sociated with better survival. Furthermore, hypermethylation of C11orf87 was also frequently observed in other GI cancers, as compared to their adjacent normal tissues. These results suggested that C11orf87 methylation may serve as a biomarker for diagnosis and prognosis of GI cancers, including gastric cancer. We further postulated that constitutive activation of STAT3 might be able to epigenetically silence C11orf87 as a possible negative feedback mechanism to protect the cells from the overactivation of STAT3. Targeted inhibition of STAT3 may not be appropriate in gastric cancer patients with promoter hypermethylation of C11orf87.
View on the web

Nasal Septal Swell Body: A Distinctive Structure in the Nasal Cavity

xlomafota13 shared this article with you from Inoreader

pubmed-meta-image.png

Ear Nose Throat J. 2021 Apr 21:1455613211010093. doi: 10.1177/01455613211010093. Online ahead of print.

ABSTRACT

OBJECTIVES: The nasal septal swell body (NSB), also known as the nasal septal turbinate, is located in the anterior part of the nasal septum. This study is a narrative review of the existing knowledge on recent developments in NSB.

METHODS: A literature search was performed using PubMed, Embase, Web of Science, Ovid, and Cochrane Library databases. Google Sc holar was used to access more extensive literature. The inclusion criteria were human studies published in English. The exclusion criteria were non-English language and animal studies.

RESULTS: Of the 345 articles that were initially obtained from 5 databases and Google Scholar, 28 were included in this review. There have been many names for NSBs in the past, which still have no unified terminology recognized by professionals. Pathological investigations revealed that NSB contains a certain amount of sinusoidal blood components. Nasal septal swell body is closely related to the internal nasal valve. Imaging studies have found that the size of NSB is associated with nasal diseases, and NSB hypertrophy can cause anatomic obstruction. In recent years, several procedures for NSB have been reported, and preliminary effectiveness has been achieved. However, the long-term outcomes of volume reduction techniques remain unproven.

CONCLUSIONS: The NSB is a distinct anatomic struct ure that may contribute to nasal obstruction and may be reduced surgically with unclear long-term results. Although being investigated for over a century, the unique physiological roles of NSB are not yet fully understood. More evidence is needed to elucidate its physiological effects.

PMID:33881954 | DOI:10.1177/01455613211010093

View on the web

Olfactory Cleft Opacification in COVID-19 Related Smell Loss: CT Findings and Correlation With Objective Testing

xlomafota13 shared this article with you from Inoreader

pubmed-meta-image.png

Ear Nose Throat J. 2021 Apr 21:1455613211011285. doi: 10.1177/01455613211011285. Online ahead of print.

ABSTRACT

OBJECTIVES: Besides the common symptoms of the coronavirus disease 2019 (COVID-19) including fever, shortness of breath, and cough, a "sudden loss of smell" has recently been added as a diagnostic symptom. The relationship between paranasal sinus computed tomography (PNS CT) and sudden loss of smell in COVID-19 was examined.

MATERIALS AND METHODS: Two groups were selected for the study, the COVID-19 and the control groups. The control group consisted of 40 patients who applied to our clinic with headache and therefore underwent PNS CT. The other group consisted of 40 patients with COVID-19 who were diagnosed with sudden loss of smell with the Connecticut Chemosensory Clinical Research Center (CCCRC) olfactory test. Clinical and demographic characteristics, tomography results, and olfactory test scores of patients with COVID-19 loss of smell and control group patients were recorded. The relationship between CT changes in the olfactory cleft and the degree of loss of smell was evaluated. The "Opacification in the olfactory cleft" was accepted as a positive CT finding.

RESULTS: Comparison of patients with COVID-19 who had a loss of smell and the control group indicated that a significant difference was observed in terms of CT findings (P = .022). When we evaluated the paranasal CTs obtained from our patients with loss of smel l, the CT of 13 patients showed pathological findings (P < .05). As the COVID-19 progressed (pneumonia and respiratory failure), the degree of loss of smell increased (P < .05). A statistically significant relationship was found between the CCCRC score and the presence of PNS CT findings (P = .0012).

CONCLUSION: The PNS CT findings are significant in patients with COVID-19 with a loss of smell and were significantly associated with the degree of loss of smell. In patients with olfactory loss due to COVID-19, PNS CT can help in diagnosis. However, for this imaging to be diagnostic, a larger patient series is needed.

PMID:33881955 | DOI:10.1177/01455613211011285

View on the web

Laryngeal Sarcoidosis

xlomafota13 shared this article with you from Inoreader

pubmed-meta-image.png

Ear Nose Throat J. 2021 Apr 21:1455613211012583. doi: 10.1177/01455613211012583. Online ahead of print.

NO ABSTRACT

PMID:33881956 | DOI:10.1177/01455613211012583

View on the web

Paeoniflorin suppresses allergic and inflammatory responses by promoting autophagy in rats with urticaria

xlomafota13 shared this article with you from Inoreader

Exp Ther Med. 2021 Jun;21(6):590. doi: 10.3892/etm.2021.10022. Epub 2021 Apr 8.

ABSTRACT

Paeoniflorin (PF) has been reported to be effective against several skin disorders, such as allergic contact dermatitis and psoriasis; however, it remains unclear whether PF can protect against urticarial lesions. Herein, the effects of PF on rats with urticarial lesions and the possible underlying mechanism were investigated. The effects of PF administration on a rat model of ovalbumin-induced urticarial-like lesions were evaluated via pathological analysis using hematoxylin-eosin staining. Toluidine blue staining was performed to detect mast cells and ELISA was performed to determine serum histamine levels. PF-induced regulatory effects on autophagic activity and the potential underlying mechanism of this were also investigated using transmission electron microscopy, immunohistochemistry and reverse transcription-quantitative PCR. It was demonstr ated that PF suppressed allergic and inflammatory responses to improve urticarial lesions, as evidenced by the attenuation of pathological abnormalities, mast cell infiltration and histamine secretion. Mechanistically, PF treatment was found to markedly limit the production and release of inflammatory cytokine interleukin (IL)-23, while the levels of IL-17 remained unchanged. PF intervention led to an increased number of autophagosomes, along with higher levels of light chain 3B (LC3B) and Beclin-1, and lower levels of P62, indicating that PF could augment autophagic activity in urticarial lesions. PF treatment increased the expression of liver kinase B1 (LKB1) and AMP-activated protein kinase-α (AMPK-α), contributing to the PF-enhanced autophagic activity. In conclusion, PF could effectively improve urticarial lesions by inhibiting inflammatory cytokine IL-23 and increasing the autophagic activity via the LKB1/AMPK-α pathway.

PMID:33884028 | PMC:PMC8056118 | DOI:10.3892/etm.2021.10022

View on the web

Microcirculatory disturbance in acute liver injury

xlomafota13 shared this article with you from Inoreader

Exp Ther Med. 2021 Jun;21(6):596. doi: 10.3892/etm.2021.10028. Epub 2021 Apr 9.

ABSTRACT

Microcirculatory disturbance is thought to be involved in the pathogenesis of acute liver injury (ALI). The current study examined the pathophysiologic role of hepatic microcirculatory disturbance in patients with ALI and in mouse models of ALI. Using serum aminotransferase (ALT)/lactate dehydrogenase (LDH) ratio as a hypoxic marker, 279 patients with ALI were classified into the low ALT/LDH ratio (ALT/LDH ≤1.5) and high ALT/LDH ratio group (ALT/LDH >1.5). In the low ALT/LDH ratio group, serum ALT, LDH, fibrinogen degradation products and prothrombin time-international normalized ratio were increased relative to the high ALT/LDH ratio group. Histologically, hepatic expression of tissue factor (TF) and hypoxia-related proteins was enhanced in the low ALT/LDH ratio group, and this was accompanied by sinusoidal fibrin deposition. Sinusoidal hyper coagulation and intrahepatic hypoxia was also analyzed in two different mouse models of ALI; Concanavalin A (ConA) mice and Galactosamine/tumor necrosis factor (TNF)-α (G/T) mice. Serum ALT/LDH ratio in ConA mice was significantly lower compared with G/T mice. Pimonidazole staining revealed the upregulation of hypoxia-related proteins in ConA mice. Recombinant human soluble thrombomodulin improved liver damage in ConA mice in association with reduced sinusoidal hypercoagulation and intrahepatic hypoxia. The present study provides evidence that serum ALT/LDH ratio aids in the identification of patients with ALI and intrahepatic hypoxia as a result of microcirculatory disturbance. The results facilitate the improved understanding of the pathogenesis of ALI, thereby offering a novel therapeutic strategy against ALI, which arises from sinusoidal hypercoagulation.

PMID:33884034 | PMC:PMC8056117 | DOI:10.3892/etm.2021.10028

View on the web

Downregulation of miR-588 is associated with tumor progression and unfavorable prognosis in patients with osteosarcoma

xlomafota13 shared this article with you from Inoreader

Exp Ther Med. 2021 Jun;21(6):592. doi: 10.3892/etm.2021.10024. Epub 2021 Apr 8.

ABSTRACT

Osteosarcoma (OS) is a primary malignant tumor characterized by a high metastatic potential and poor prognosis. The dysregulation of miR-588 has been demonstrated to serve crucial roles in the progression of numerous types of cancer. The present study aimed to investigate the expression and function of miR-588 in the development of OS. To do so, clinical samples were collected and analyzed, and in vitro experiments were conducted. A total of 104 patients with OS were recruited between 2012 and 2014. The expression of miR-588 was analyzed by reverse transcription quantitative PCR. The association between miR-588 expression and the clinicopathological characteristics and survival rate of patients with OS was evaluated. Furthermore, Cell Counting Kit-8 and Transwell assays were used to evaluate the effect of miR-588 on the proliferation and the migrat ory and invasive abilities of various OS cell lines. The results demonstrated that miR-588 expression in OS tissues and cells was significantly lower compared with normal tissues and cells. In addition, miR-588 expression was closely associated with the Musculoskeletal Tumor Society (MSTS) staging of patients with OS. miR-588 expression and MSTS staging were therefore considered as independent indicators for the prognosis of patients with OS. In addition, miR-588 downregulation significantly stimulated the proliferation and migratory and invasive abilities of OS cells. Taken together, these findings indicated that miR-588 may serve as an independent prognostic factor and tumor suppressor in OS.

PMID:33884030 | P MC:PMC8056108 | DOI:10.3892/etm.2021.10024

View on the web

Dl-butylphthalide inhibits rotenone-induced oxidative stress in microglia via regulation of the Keap1/Nrf2/HO-1 signaling pathway

xlomafota13 shared this article with you from Inoreader

Exp Ther Med. 2021 Jun;21(6):597. doi: 10.3892/etm.2021.10029. Epub 2021 Apr 9.

ABSTRACT

Activated microglia are a source of superoxide which often increases oxidative stress in the brain microenvironment, increase production of reactive oxygen species (ROS) and directly or indirectly lead to dopaminergic neuronal death in the substantia nigra. Thus superoxide contributes to the pathogenesis of Parkinson's disease (PD). Evidence suggests that mitochondria are the main source of ROS, which cause oxidative stress in cells. Levels of ROS are thus associated with the function of the mitochondrial complex. Therefore, protecting the mitochondrial function of microglia is important for the treatment of PD. Dl-butylphthalide (NBP), a compound isolated from Chinese celery seeds, has been approved by the China Food and Drug Administration for the treatment of acute ischemic stroke. Recently, NBP demonstrated therapeutic potential for PD. However , the mechanism underlying its neuroprotective effect remains unclear. The present study aimed to investigate the effect of NBP on rotenone-induced oxidative stress in microglia and its underlying mechanisms. The results demonstrated that NBP treatment significantly increased mitochondrial membrane potential and decreased ROS level in rotenone-induced microglia. Western blot analysis showed that NBP treatment promoted entry of nuclear respiratory factor-2 (Nrf2) into the nucleus, increased heme oxygenase-1 (HO-1) expression and decreased the level of the Nrf2 inhibitory protein, Kelch-like ECH-associated protein 1. Overall, the findings indicated that NBP inhibited rotenone-induced microglial oxidative stress via the Keap1/Nrf2/HO-1 pathway, suggesting that NBP may serve as a novel agent for the treatment of PD.

PMID:33884035 | PMC:PMC8056112 | DOI:10.3892/etm.2021.10029

View on the web

Interferon-τ regulates the expression and function of bovine leukocyte antigen by downregulating bta-miR-204

xlomafota13 shared this article with you from Inoreader

Exp Ther Med. 2021 Jun;21(6):594. doi: 10.3892/etm.2021.10026. Epub 2021 Apr 8.

ABSTRACT

IFN-τ is a pregnancy recognition factor that regulates embryo implantation in ruminants. IFN-τ has been suggested to be involved in the expression of microRNA (miRNA/miR) and bovine leukocyte antigen (BoLA), which is an analog of the human major histocompatibility complex class I. However, little is known about whether the miRNAs are involved in the expression of BoLA in ruminants. The present study firstly verified that bta-miR-204 was downregulated and that BoLA was upregulated in the uterine tissues of dairy cows during early pregnancy. Subsequently, luciferase reporter assays, reverse transcription-quantitative PCR and western blot analysis were used to validate BoLA as the target gene of bta-miR-204. Moreover, BoLA was markedly upregulated and bta-miR-204 was downregulated in bovine endometrial epithelial cells (bEECs) treated with IFN-τ. I n addition, the results indicated that when the expression level of BoLA was increased by IFN-τ, the expression level of programmed death-ligand 1 (PD-L1) and programmed death-ligand 2 (PD-L2) was also increased. Furthermore, when BoLA was silenced in bEECs by small interfering RNA, the expression of PD-L1 and PD-L2 was not affected by IFN-τ. The expression level of PD-L1 and PD-L2 was also increased in the uterine tissues of pregnant dairy cattle. In conclusion, IFN-τ may function by suppressing the expression of bta-miR-204 to increase the expression of BoLA during the embryo implantation period in cattle. IFN-τ may induce PD-L1 and PD-L2 transcription by regulating BoLA, which may influence the T cell immune response, thereby regulating pregnant cattle immunization.

PMID:33884032 | PMC:PMC8056107 | DOI:10.3892/etm.2021.10026

View on the web

Αναζήτηση αυτού του ιστολογίου