CX3CR1+ macrophages interact with hepatic stellate cells to promote hepatocellular carcinoma through CD8+ T cell suppression.

BACKGROUND AND AIMS: Hepatic stellate cells (HSCs) contribute to hepatocellular carcinoma (HCC) progression by regulating multiple factors. However, the entire immunoregulatory functions of HSCs are still obscure. Here, we aim to investigate whether HSCs impose CX3CR1+ macrophages to pro-tumorigenic properties in the peritumoral area. APPROACH AND RESULTS: In single cell RNA-sequencing analysis of HCC patients, a subpopulation of macrophages specifically expressed Arg1 and Cx3cr1 in the peritumoral area, and were highly enriched with retinol metabolism-related genes. Flow cytometry analysis showed significantly increased frequencies of CD14+CD11b+HLA-DR‒ macrophages with CX3CR1 in the HCC adjacent region where α-SMA-expressing activated HSCs (aHSCs) showed co-localized expression of CX3CL1. Accordingly, in tumor-bearing mice, Cx3cl1 mRNA expression was notably increased in aHSCs within the adjacent HCC, where infiltration of CX3CR1+Ly6C+ macrophages was mostly observed with decreased CD8+ T cells. In adoptive transfer and in vitro co-culture of myeloid cells, we demonstrated that CX3CR1+Ly6C+ macrophages migrated and highly expressed arginase-1 by interacting with retinoid-enriched aHSCs in the adjacent HCC. Direct treatment of retinoids or co-culturing with retinol-storing mouse aHSCs or human LX-2 cells significantly increased arginase-1 expression in CX3CR1+Ly6C+ macrophages and human blood CD14+ cells, leading to the suppression of CD8+ T cell proliferation. Moreover, genetic deficiency of CX3CR1 in myeloid cells or pharmacological inhibition of retinol metabolism remarkably attenuated HCC development. CONCLUSION: We showed that CX3CR1+Ly6C+ macrophages migrate and interact with aHSCs in the peritumoral region where retinoids induce arginase-1 expression in CX3CR1+Ly6C+ macrophages, subsequently depriving CD8+ T cells of arginine and promoting HCC.

Modulation of synaptic transmission through O-GlcNAcylation.

O-GlcNAcylation is a posttranslational modification where N-acetylglucosamine (O-GlcNAc) is attached and detached from a serine/threonine position by two enzymes: O-GlcNAc transferase and O-GlcNAcase. In addition to roles in diabetes and cancer, recent pharmacological and genetic studies have revealed that O-GlcNAcylation is involved in neuronal function, specifically synaptic transmission. Global alteration of the O-GlcNAc level does not affect basal synaptic transmission while the effect on synaptic plasticity is unclear. Although synaptic proteins that are O-GlcNAcylated are gradually being discovered, the mechanism of how O-GlcNAcylated synaptic protein modulate synaptic transmission has only been reported on CREB, synapsin, and GluA2 subunit of AMPAR. Future research enabling the manipulation of O-GlcNAcylation in individual synaptic proteins should reveal hidden aspects of O-GlcNAcylated synaptic proteins as modulators of synaptic transmission.

Cutaneous Layer and SMAS Suspension (CaSS) Lift as a Minimally Invasive Lateral Midface Lift.

BACKGROUND: In our prior study, the authors determined that pulling on the superficial adipose layer is more effective in lifting the skin than pulling on the superficial musculoaponeurotic system (SMAS). Applying this concept of using the superficial adipose layer to transmit the lifting force to the skin, this study examined improvements in patients who underwent lateral midface lifting using our minimally invasive multilayer lifting technique and measured the duration of those improvements. METHODS: Along the hairline in front of the sideburns, a W-shaped zigzag incision of 3 to 8 mm in width and 3 to 4 cm in length was made. On the temporal scalp, 3 to 4 cm away from the first incision, a second incision was made more lateral/posterior to the first incision, and an elliptical excision of 3 to 5 mm in width and 3 to 4 cm in length was made. From the medial cut margin of the anterior first incision, the superficial temporal fascia/SMAS (the deep layer), and the superficial adipose layer (the superficial layer) were purchased with 3-0 polyester sutures, tunneled under the soft tissue, and fixed to the deep temporal fascia of the second posterior temporal incision. Prior to the excised temporal scalp closure, the dermis in the medial cut margin of the second incision was pulled to the rear as much as possible and fixed to the deep temporal fascia. RESULTS: The effects of surgery were monitored for 6 to 42 months after surgery. The nasolabial folds were improved. Skin elasticity also showed significant improvements, which lasted throughout the follow-up period (up to 42 mo). CONCLUSIONS: Unlike traditional wide dissection SMAS facelift, our method requires minimal incisions and does not require skin undermining. Therefore, the operating time is shorter, and postoperative swelling is minimized. In our technique, the superficial adipose layer, the superficial temporal fascia/SMAS, and the dermis were pulled individually to lift all layers of the lateral midface soft tissues. This results in a significant and long-lasting lateral midface rejuvenation.

Anti­tumor properties of FoxO1 in YD­9 oral squamous cell carcinoma cells.

Oral squamous cell carcinoma (OSCC) is a tumor with a poor prognosis and a high recurrence rate. Despite its high annual incidence worldwide, appropriate therapeutic strategies have not yet been developed. Consequently, the 5­year survival rate for OSCC is low when advanced stages or recurrence is diagnosed. Forkhead transcriptional factor O1 (FoxO1) is a key mediator for maintaining cellular homeostasis. FoxO1 can function as a tumor suppressor as well as an oncogene depending on the cancer type. Therefore, the precise molecular functions of FoxO1 need to be validated, considering intracellular factors and the extracellular environment. To the best of our knowledge, however, the roles of FoxO1 in OSCC have not yet been defined. The present study examined FoxO1 levels under pathological conditions (oral lichen planus and oral cancer) and selected an appropriate OSCC cell line (YD­9). Crispr/Cas9 was used to generate FoxO1­deficient YD­9 cells in which the protein levels of phospho ERK and phospho STAT3 were upregulated, promoting cancer proliferation and migration. In addition, FoxO1 reduction increased the levels of the cell proliferation markers phospho H3 (Ser10) and PCNA. FoxO1 loss significantly reduced cellular ROS levels and apoptosis in YD­9 cells. Collectively, the present study demonstrated that FoxO1 exerted an anti­tumor effect by suppressing proliferation and migration/invasion but promoting oxidative stress­linked cell death in YD­9 OSCC cells.

Sexually Transmitted Infections & the Heart.

Sexually transmitted infections (STIs) have substantial morbidity and mortality worldwide, with over 1 million new infections occurring daily. Similarly, cardiovascular (CV) disease is the leading global cause of death and has tremendous impact on disability as well as quality of life. Several STIs have potential CV consequences and may precipitate reoccurrence of underlying CV comorbidity. Notably, untreated STIs and associated CV complications have an increased impact on marginalized individuals and those with limited access to health resources and care. Syphilis, human immunodeficiency virus, human papillomavirus, herpes simplex virus, hepatitis B, hepatitis C, cytomegalovirus, chlamydia, gonorrhea, and trichomoniasis have been identified as having CV implications. Yet, the data linking compromised CV health and STIs have not previously been summarized. The present review encapsulates the current knowledge surrounding the impacts of STIs on CV health as well as diagnostic and treatment strategies.

FoxO1 Controls Redox Regulation and Cellular Physiology of BV-2 Microglial Cells.

Microglia are brain-resident macrophage-like cells that play critical roles in diverse pathophysiological conditions, including development, neurogenesis, tissue damage, and pathogenic infection. Identifying molecular switches that govern the fate and function of microglia would be valuable for maintaining brain homeostasis. Forkhead box protein O1 (FoxO1) is the first identified gene in the FoxO family and serves as a potent transcriptional regulator that participates in development, apoptosis, metabolism, and stress response. It has been recently reported that FoxO1 expression is downregulated in human microglia with age, but the role of FoxO1 has not been characterized so far. In the present study, we investigated the molecular function of FoxO1 in microglia by utilizing BV-2 cells. By generating FoxO1-deficient BV-2 microglia through Crispr/Cas9 system, we analyzed the influence of FoxO1 on redox status, metabolism, and polarization of microglia. Our data clearly showed that FoxO1 deficiency suppressed oxidative stress and cell death. In addition, FoxO1 level could modulate metabolic status and polarizing potential of BV-2 microglia. FoxO1 might be a critical element for the regulation of microglial cell physiology and the maintenance of the brain homeostasis.

Snakebite Envenomation and Heart: Systematic Review.

Snakebite envenomation is a neglected tropical disease which can result in morbidity and mortality. Cardiac implications are poorly understood due to the low frequency of cardiotoxicity combined with a lack of robust information, as snakebites commonly occur in remote and rural areas. This review aims to assess cardiovascular implications of snakebite envenoming and proposes an algorithm for screening of cardiovascular manifestations. A systematic review was performed and 29 articles relating to cardiovascular involvement in snakebite envenomation were selected. Cardiovascular involvement seems to be rare and includes a wide spectrum of outcomes, such as myocardial infarction, ventricular dysfunction, hypotension, cardiac arrest, and myocarditis. In a significant proportion of the cases analyzed (24.39%), the cardiovascular manifestations had major consequences (cardiac arrest, myocardial infarction, malignant ventricular arrhythmias, or death). Clinical monitoring, physical examination, and early electrocardiogram should be considered as key measures to detect cardiovascular involvement in patients with evidence of systemic illness.

Ginsenoside F2 induces cellular toxicity to glioblastoma through the impairment of mitochondrial function.

BACKGROUND: Glioblastoma (GBM) is the most aggressive tumor residing within the central nervous system, with extremely poor prognosis. Although the cytotoxic effects of ginsenoside F2 (GF2) on GBM were previously suggested, the precise anti-GBM mechanism of GF2 remains unclear. The aim of this study was to explore the anti-cancer molecular mechanism of GF2 toward human GBM. METHODS: GF2-driven cellular toxicity was confirmed in two different GBM cells, U373 and Hs683. To test mitochondrial impairment driven by GF2, we examined the mitochondrial membrane potential, OCR, and ATP production. An intracellular redox imbalance was identified by measuring the relative ratio of reduced glutathione to oxidized glutathione (GSH/GSSG), glutaredoxin (GLRX) mRNA expression, intracellular NAD+ level, and AMPK phosphorylation status. RESULTS: GF2 increased the percentage of cleaved caspase 3-positive cells and γH2AX signal intensities, confirming that GF2 shows the cytotoxicity against GBM. GO enrichment analysis suggested that the mitochondrial function could be negatively influenced by GF2. GF2 reduced the mitochondrial membrane potential, basal mitochondrial respiratory rate, and ATP production capacity. Our results showed that GF2 downregulated the relative GSH/GSSG, intracellular NAD+ level, and GLRX expression, suggesting that GF2 may alter the intracellular redox balance that led to mitochondrial impairment. CONCLUSION: GF2 reduces mitochondrial membrane potential, inhibits cellular oxygen consumption, activates AMPK signaling, and induces cell death. Our study examined the potential vulnerability of mitochondrial activity in GBM, and this may hold therapeutic promise.

Multiple Functions of Fubp1 in Cell Cycle Progression and Cell Survival.

The discovery of novel and critical genes implicated in malignant development is a topic of high interest in cancer research. Intriguingly, a group of genes named "double-agent" genes were reported to have both oncogenic and tumor-suppressive functions. To date, less than 100 "double-agent" genes have been documented. Fubp1 is a master transcriptional regulator of a subset of genes by interacting with a far upstream element (FUSE). Mounting evidence has collectively demonstrated both the oncogenic and tumor suppressive roles of Fubp1 and the debate regarding its roles in tumorigenesis has been around for several years. Therefore, the detailed molecular mechanisms of Fubp1 need to be determined in each context. In the present study, we showed that the Fubp1 protein level was enriched in the S phase and we identified that Fubp1 deficiency altered cell cycle progression, especially in the S phase, by downregulating the mRNA expression levels of Ccna genes encoding cyclin A. Although this Fubp1-cyclin A axis appears to exist in several types of tumors, Fubp1 showed heterogeneous expression patterns among various cancer tissues, suggesting it exhibits multiple and complicated functions in cancer development. In addition, we showed that Fubp1 deficiency confers survival advantages to cells against metabolic stress and anti-cancer drugs, suggesting that Fubp1 may play both positive and negative roles in malignant development.

A case report of a tongue ulcer presented as the first sign of occult tuberculosis.

BACKGROUND: Tuberculosis (TB) is a serious infectious disease with considerable fatality, typically affecting the pulmonary system and, rarely, other body organs including the oral cavity. Due to the rarity of oral TB, it is frequently overlooked in differential diagnosis of oral lesions. Despite a declining trend in TB incidence in recent years, it is still a major public health problem with high contagiousness, thereby requiring the early diagnosis and prompt treatment. CASE PRESENTATION: A 57-year-old male patient presented with chief complaint of painful ulcer on tip of his tongue. He reported that the ulcer developed without any remarkable event such as mechanical trauma, vesicle formation or systemic illness. His past medical history revealed the TB over 40 years ago, which had reportedly healed after pharmacological treatments. As the ulceration persisted after topical steroid application and careful education about avoiding possible mechanical stimuli, biopsy was performed and histological finding showed typical findings of oral tuberculosis including intense granulomatous inflammatory features with small red rods of mycobacterial organisms as well as epithelioid cells and Langhans giant cells. After suitable antituberculosis treatments, oral tuberculosis ulcer was almost completely healed. We present a case of oral TB affecting tip of the tongue in a patient with a history of pulmonary TB and emphasize the understanding of intraoral manifestations for early diagnosis and prompt treatment of TB. CONCLUSIONS: The present case represented the importance of understanding oral tuberculosis manifestations for dental clinicians who might be frequently the first health care professionals to encounter various oral lesions.

Focal localization of inflammatory cytokines and neurotrophins in a tongue chronic injury model.

OBJECTIVES: Chronic injury in tongue causes the variety of reactions in the oral cavity, frequently leading to its functional and structural disintegrity including inflammation and sensory dysfunction, but its detailed profiles were not elucidated yet. One of the chronically injured tongue such as tongue piercing, as a pathological aspect, is currently popular among younger people but may be associated with severe side effects, leading to pathophysiological complications. However, the pathophysiological aspects and related cellular and molecular mechanisms underlying tongue injury are not clearly understood. DESIGN: In this study, we designed an experimental model system using C57BL/6 male mice that mimics a chronically injured situation by penetrating the middle part of tongue with silk suture. After 5 and 10 days mice were sacrificed and tongues were collected and processed for histological evaluation and immunohistochemistry. RESULTS: We found that the anterior tongue showed localization of neuro-inflammatory signaling molecules such as myeloperoxidase (MPO), matrix metalloproteinase 2 (MMP2), tumor necrosis factor-α (TNF-α), nerve growth factor, and transient receptor potential cation channel subfamily V member 1 (TRPV1) without any apparent inflammation in temporal manner. In addition, the signal for AM1-43, an activity-dependent nerve terminal probe, decreased within the fungiform papillae on the anterior tongue after injury. CONCLUSIONS: These results implied that the distinct localizations of inflammatory cytokines and neurotrophin would contribute altered sensory function in anterior tongue following the chronic injury. Our study indicates the possible pathophysiologic mechanism underlying neuro-inflammation following chronically injury of tongue. In addition, it could be cautiously postulated that mechanical injury should be avoided to prevent chronic pain disorders from being triggered.

CX3CR1 differentiates F4/80low monocytes into pro-inflammatory F4/80high macrophages in the liver.

The expression of chemokine receptor CX3CR1 is related to migration and signaling in cells of the monocyte-macrophage lineage. The precise roles of CX3CR1 in the liver have been investigated but not clearly elucidated. Here, we investigated the roles of CX3CR1 in hepatic macrophages and liver injury. Hepatic and splenic CX3CR1lowF4/80low monocytes and CX3CR1lowCD16- monocytes were differentiated into CX3CR1highF4/80high or CX3CR1highCD16+ macrophages by co-culture with endothelial cells. Moreover, CX3CL1 deficiency in human umbilical vein endothelial cells (HUVECs) attenuated the expression of interleukin-1ß (IL-1ß) and tumor necrosis factor-α (TNF-α), whereas recombinant CX3CL1 treatment reversed this expression in co-cultured monocytes. Upon treatment with clodronate liposome, hepatic F4/80high macrophages were successfully depleted at day 2 and recovered similarly in CX3CR1+/GFP and CX3CR1GFP/GFP mice at week 4, suggesting a CX3CR1-independent replacement. However, F4/80high macrophages of CX3CR1+/GFP showed a stronger pro-inflammatory phenotype than CX3CR1GFP/GFP mice. In clodronate-treated chimeric CX3CR1+/GFP and CX3CR1GFP/GFP mice, CX3CR1+F4/80high macrophages showed higher expression of IL-1ß and TNF-α than CX3CR1-F4/80high macrophages. In alcoholic liver injury, despite the similar frequency of hepatic F4/80high macrophages, CX3CR1GFP/GFP mice showed reduced liver injury, hepatic fat accumulation, and inflammatory responses than CX3CR1+/GFP mice. Thus, CX3CR1 could be a novel therapeutic target for pro-inflammatory macrophage-mediated liver injury.

Kv3.1 and Kv3.4, Are Involved in Cancer Cell Migration and Invasion.

Voltage-gated potassium (Kv) channels, including Kv3.1 and Kv3.4, are known as oxygen sensors, and their function in hypoxia has been well investigated. However, the relationship between Kv channels and tumor hypoxia has yet to be investigated. This study demonstrates that Kv3.1 and Kv3.4 are tumor hypoxia-related Kv channels involved in cancer cell migration and invasion. Kv3.1 and Kv3.4 protein expression in A549 and MDA-MB-231 cells increased in a cell density-dependent manner, and the pattern was similar to the expression patterns of hypoxia-inducible factor-1α (HIF-1α) and reactive oxygen species (ROS) according to cell density, whereas Kv3.3 protein expression did not change in A549 cells with an increase in cell density. The Kv3.1 and Kv3.4 blocker blood depressing substance (BDS) did not affect cell proliferation; instead, BDS inhibited cell migration and invasion. We found that BDS inhibited intracellular pH regulation and extracellular signal-regulated kinase (ERK) activation in A549 cells cultured at a high density, potentially resulting in BDS-induced inhibition of cell migration and invasion. Our data suggest that Kv3.1 and Kv3.4 might be new therapeutic targets for cancer metastasis.

Forces Required to Pull the Superficial Fascia in Facelifts.

PURPOSE: The aims of this study were to characterize the histology of the sideburn and cheek area and to measure the force required to pull the superficial fascia (SF) of Asians in facelift procedures. METHODS: The hemiface of a formalin-fixed Korean male adult cadaver (77 years old) was used to study the histology of the sideburn and cheek area. In 42 patients during facelift procedures, the force needed to pull the overlying skin at the midpoint between the sideburn and nasolabial fold 2 mm was measured using a tensiometer. RESULTS: In the cheek, the superficial fatty layer of the superficial fascia (SFS) was found to maintain its thickness throughout the region between the dermis and the membranous layer of the superficial fascia (MSF). The MSF was continuous with the superficial temporal fascia (STF). In the sideburn, the MSF and parotid fascia closely adhered to each other. The force required to move the overlying skin 2 mm when pulling the MSF (10.27 ± 3.64 N) was more than twice as great (217%) as the force required when pulling the SFS (4.73 ± 2.15 N; P < .001). The forces required when pulling the MSF and SFS to move the overlying skin 2 mm were significantly greater in the sideburn area (11.56 ± 3.37 N and 5.52 ± 2.08 N, respectively) than in the cheek area (8.97 ± 3.43 N and 5.52 ± 2.08 N, respectively; P < .001). CONCLUSION: When lifting the SF at the cheek or sideburn area, lifting the SFS requires less tension than MSF to move the overlying skin. In the cheek area, less tension is needed to move the overlying skin than in the sideburn area.

OBJECTIF: La présente étude visait à caractériser l'histologie de la zone des favoris et des joues et à mesurer la force nécessaire pour tirer le fascia superficiel (FS) lors du redrapage du visage et du cou de visages asiatiques. MÉTHODOLOGIE: Les chercheurs ont utilisé l'hémiface d'un cadavre adulte coréen de sexe masculin de 77 ans fixé dans le formol pour étudier l'histologie des régions des favoris et des joues. Chez 42 patients pendant un redrapage du visage et du cou, les chercheurs ont mesuré la force nécessaire pour tirer la peau sus-jacente de 2 mm au point médian entre les favoris et le pli nasolabial à l'aide d'un tensiomètre. RÉSULTATS: Dans les joues, les chercheurs ont découvert que la couche de graisse superficielle du fascia superficiel (GFS) conservait son épaisseur dans toute la région entre le derme et la couche membraneuse du fascia superficiel (MFS). La MFS était continue avec la GFS. Dans les favoris, la MFS adhérait étroitement au fascia de la parotide. Les forces nécessaires pour déplacer la peau sus-jacente de 2 mm en tirant sur la MFS (10,27 ± 3,64 N) étaient plus de deux fois plus élevées (217 %) que celles nécessaires pour tirer la GFS (4,73 ± 2,15 N; P < 0,001). Les forces nécessaires pour tirer la MFS et la GSF afin de déplacer la peau sus-jacente de 2 mm étaient considérablement plus élevées dans la région des favoris (11,56 ± 3,37 N et 5,52 ± 2,08 N, respectivement) que dans celle des joues (8,97 ± 3,43 N et 5,52 ± 2,08 N, respectivement) (P < 0,001). CONCLUSIONS: Lorsque le FS est soulevé dans la région des favoris ou des joues, il faut moins de tension pour soulever la GFS que la MFS pour tendre la peau sus-jacente. Dans la région des joues, il faut moins de tension pour déplacer la couche de peau supérieure que dans la région des favoris.

Comparison of wound healing effects between Oncorhynchus keta-derived polydeoxyribonucleotide (PDRN) and Oncorhynchus mykiss-derived PDRN.

BACKGROUND: Polydeoxyribonucleotide (PDRN) influencing cellular growth and differentiation is recognized to promote wound healing by stimulating tissue repair. Although PDRN can be extracted from human placentas, PDRN medications have recently been extracted from the semen of trout (Oncorhynchus mykiss) and salmon (Oncorhynchus keta). The present study was designed to evaluate the wound healing effects of O. keta-derived PDRN for injection (Rejuvenex) and PDRN cream (Rejuvenex Cream) in comparison with those of O. mykiss-derived PDRN injection (Placentex). METHODS: Full-thickness skin defects were made on the back of mice (n=60). The mice were divided into the following four groups according to the dressing used for the wounds: O. mykiss-derived PDRN injection group, O. keta-derived PDRN injection group, O. keta-derived PDRN cream group, and normal saline soaked dressing group (control group). We analyzed the gross findings, wound sizes, histological findings, immunohistochemistry and enzyme-linked immunosorbent assays for the groups immediately after the treatment, and again after 4, 7, and 10 days of treatment. RESULTS: The wound healing effects were the greatest in the O. keta-derived PDRN injection and O. mykiss-derived PDRN injection groups, which showed similar scores, followed by the O. keta-derived cream and normal saline soaked dressing groups. CONCLUSION: The injection of PDRN extracted from O. keta was found to be as effective at healing full-thickness skin defects as the O. mykiss-derived PDRN injection, which is currently used in the clinic. Moreover, the O. keta-derived PDRN injection was also found to reduce the time required for wound healing.

Cellular toxicity driven by high-dose vitamin C on normal and cancer stem cells.

As a powerful antioxidant, vitamin C protects cells from oxidative damage by inhibiting production of free radicals. However, high levels of vitamin C shows cytotoxicity especially on cancerous cells through generating excessive ROS and blocking the energy homeostasis. Although the double-sided character of vitamin C has been extensively studied in many cell types, there is little research on the consequence of vitamin C treatment in stem cells. Here, we identified that high-dose vitamin C shows cellular toxicity on proliferating NSPCs. We also demonstrated that undifferentiated NSPCs are more sensitive to vitamin C-driven DNA damage than differentiated cells, due to higher expression of Glut genes. Finally, we showed that high-dose vitamin C selectively induces DNA damage on cancer stem cells rather than differentiated tumor cells, raising a possibility that vitamin C may be used to target cancer stem cells.

Mixed Tumor in Deep Lobe and Versatility of Acellular Dermal Matrix.

Frey's syndrome and infra-auricular depressed deformities are the ones of the most common complications that can occur after total parotidectomy. We report 1 case of pleomorphic adenoma occurred in the deep lobe that obtained good results from using acellular dermal matrix (ADM) after total parotidectomy. A 24-year-old man visited the hospital with oval shape mass in right mandibular angle which of 4 cm in size was found in the deep lobe of right parotid gland from Magnetic resonance imaging scanning and a pleomorphic adenoma was suspected. A total parotidectomy was performed while preserving the facial nerve. The material known as ADM were placed in the depressed part from where the mass was removed, and the site was sutured. The surgery site was healed well without any complications such as Frey's syndrome or infra-auricular depressed deformities. The pathological result was confirmed as pleomorphic adenoma. In addition to these advantages, it does not have little potential of deformation by the gravity after the surgery, and there is no restraint on circulation, which makes fabrication free and each deformation into various shapes can be described as another advantage of the reconstruction using the ADM.

Levator Aponeurosis and Muller Muscle Plication Reinforced With Levator Sheath Advancement for Blepharoptosis Correction.

The authors innovated the levator aponeurosis and Muller muscle plication reinforced with levator sheath advancement (AMPSA) for blepharoptosis correction. The orbital septum was opened 1 mm above its fusion with the levator aponeurosis. The preaponeurotic fat was retracted and the thickened part of the levator sheath was identified. Two plication sutures were made: medial suture at the medial border of the pupil and lateral between the lateral border of the pupil and the lateral limbus. A needle with 6-0 nylon thread first bit the tarsal plate approximately 1 mm below its upper border, then bit the levator aponeurosis and the Muller muscle together at 3 to 6 mm above the upper border of the tarsal plate. The needle bit 1 to 3 mm of the thickened part of the levator sheath and the suture was tied. A total of 116 eyes were operated on using levator aponeurosis and Muller muscle plication (AMP), and 79 eyes using AMPSA. The mean follow-up period was 11.4 months. In the AMP group, the postoperative marginal reflex distance-1 (MRD-1) (3.8 ±â€Š0.2 mm) was significantly greater than the preoperative MRD-1 (2.7 ±â€Š0.3 mm) (P < 0.001). In the AMPSA group, the postoperative MRD-1 (3.5 ±â€Š0.3 mm) was also significantly greater than the preoperative MRD-1 (1.7 ±â€Š0.4 mm) (P < 0.001). The improvement in MRD-1 was greater in the AMPSA group (1.7 ±â€Š0.4 mm) than in the AMP group (1.1 ±â€Š0.3 mm) (P < 0.001). The difference in the MRD-1 outcome between AMPSA and AMP (0.6 mm) was obtained by advancing the thickened part of the levator sheath. AMPSA may be an effective procedure for correcting blepharoptosis.

Osteomyelitis following Domestic Animal Bites to the Hand: Two Case Reports and Practical Guidelines.

Recently, the number of cases of animal bite wounds has increased significantly in concordance with an increase in the pet population around the world. The authors report two rare cases of osteomyelitis of the phalanx following cat and dog bites. On initial physical examination, signs of a severe infection were observed. Radiographs of both patients showed the presence of osteomyelitis, and in one of the patients, the diagnosis was confirmed with a bone biopsy. After use of empirical antibiotics, intravenous antibiotic therapy that matched the identified bacterium's sensitivity was initiated, and at the same time, secure dressing including debridement was performed to induce secondary healing. In addition, the patients were closely monitored with serial X-rays, and culture and blood test follow-up. One patient fully recovered without sequelae, but the other patient suffered a loss of distal interphalangeal joint motion. When dealing with bite wounds located on the hand, it is important to visit the hospital as soon as possible and receive the appropriate treatment early. Moreover, to prevent severe complications such as osteomyelitis, it is important to administer antibiotic therapy to which the cultured bacteria are sensitive, along with proper wound management and prophylactic antibiotic treatment.

Chondroid Syringoma on Face.

Chondroid syringoma is a rare mixed tumor of the skin which is composed of both mesenchymal and epithelial cells. Its incidence at less than 0.1% and is frequently located on the head and neck. Chondroid syringoma is easily confused with epidermal cysts. Since malignant forms of chondroid syringoma have been reported, accurate and timely diagnosis is important for proper management. We report clinical and histological features of chondroid syringoma in 5 patients treated at our institution. In most of the cases, chondroid syringoma presented as a round, firm, nodular or cystic lesion that had well marginated heterogeneity in sonography. Clinically, all of the lesions were removed by simple excision. Microscopically, all five tumors were well circumscribed and consisted of epithelial, myoepithelial, and stromal components. The epithelial component formed tubules lined by one or more rows of eosinophilic epithelial cells. The outer layer of tubules appeared to be flattened myoepithelial cells. The stroma is myxoid and contained spindle shaped myoepithelial cells. We expect that the clinical, sonographic, and histological data from our report may help clinicians who are confronted with various kinds of analogous facial lesions to decide the most proper management for their patients.