Case report: Rare oral manifestations in Cowden syndrome with PTEN mutation.

Background: Cowden syndrome (CS) is a rare genetic disorder associated with PTEN gene mutations. It is characterized by macrocephaly, specific mucocutaneous features, and a predisposition to benign and malignant tumors. Cases of CS primarily presenting with oral clinical manifestations are relatively uncommon. Methods/Results: We report the case of a 41-year-old male proband who presented with bilateral commissural and lingual externally projecting symmetric lesions for over two years. The proband also exhibited other features, including macrocephaly, communication difficulties, and obesity. Similar oral clinical manifestations were observed in family members. Whole exome sequencing analysis revealed PTEN gene mutations associated with CS in both the proband and his younger brother. This case serves as a reminder to be aware of the diverse presentations of CS in oral clinical practice and highlights the importance of genetic testing for guiding diagnosis and treatment. Conclusion: There are few reported cases of CS primarily presenting with oral lesions. This finding contributes to further understanding of certain aspects of the pathogenesis of CS and enhances awareness of CS cases primarily exhibiting oral clinical manifestations.

Correlation Between Rats Hippocampal ATP Content and Delayed Encephalopathy After Acute Carbon Monoxide Poisoning.

Objective: To study the correlation between the adenosine triphosphate (ATP) content in the hippocampus of rats and delayed encephalopathy after acute carbon monoxide (CO) poisoning. Methods: A total of 40 male Wistar rats weighing 180-230g, in accordance with the random number table, were selected and divided into the delayed encephalopathy after acute carbon monoxide poisoning (DEACMP: Rats with cognitive impairment after carbon monoxide poisoning) group (n = 32) and the control group (n = 8). A DEACMP rat model was generated by inhalation of CO. The Morris water maze evaluated the ability to learn and memorize in rats. The changes in neurons in the hippocampus of the rats were observed by hematoxylin-eosin (HE) staining. Lastly, the ATP content in the hippocampus of the rats was measured by high-performance liquid chromatography (HPLC). Results: The ATP content of the experimental group was significantly higher than that of the control group in the hippocampus of the rat model, so the difference was statistically significant (P < 0.05); the intra-group comparison was made for the ATP content in the experimental group, and the difference was statistically significant as group 21d > group 14d > group 7d (P < 0.05); and no significant difference was found between group 21d and group 28d (P > 0.05). Conclusion: The changes in the ATP content in the hippocampus of the rats are correlated with the occurrence of delayed encephalopathy after acute carbon monoxide poisoning; it may take part in the pathogenesis of DEACMP. This offers some elicitation to the prevention and treatment of the disease.

ERp44 Regulates the Proliferation, Migration, Invasion, and Apoptosis of Gastric Cancer Cells Via Activation of ER Stress.

Gastric cancer (GC) is one of the most prevalent malignancies worldwide. Endoplasmic reticulum (ER) stress plays a key role in the progression of GC. Rapid proliferation of tumor cells interferes with ER homeostasis, leading to ER stress and triggering unfolded protein response. Therefore, it is very necessary to investigate abnormally expressed ER resident proteins (ERp) in cancer cells. This study aimed to investigate the possible roles of ERp44. The mRNA and protein expression of genes were detected using qRT-PCR and western blot. Cell apoptosis was calculated using flow cytometry. Cell proliferation was determined using CCK-8 and colony formation assay. Cell migration was detected by wound healing, and cell invasion was measured by transwell assay. We found that ERp44 was obviously decreased in GC tissues. Furthermore, ERp44 overexpression distinctly suppressed the proliferation, migration, and invasion of MGC-803 and KATO III cells. In contrast, apoptosis was promoted by ERp44 overexpression. Furthermore, mechanistic studies revealed that overexpression of ERp44 inhibited malignant biological processes by regulating the eIF-2α/CHOP signaling pathway. Taken together, our data demonstrated that ERp44 regulated the proliferation, migration, invasion, and apoptosis via ERp44/eIF-2α/CHOP axis in GC. Targeting the ERp44and ER stress may be a promising strategy for GC.

Noninvasive diagnosis of oral squamous cell carcinoma by multi-level deep residual learning on optical coherence tomography images.

BACKGROUND: Oral Squamous Cell Carcinoma (OSCC) is one of the most severe cancers in the world, and its early detection is crucial for saving patients. There is an inevitable necessity to develop the automatic noninvasive OSCC diagnosis approach to identify the malignant tissues on Optical Coherence Tomography (OCT) images. METHODS: This study presents a novel Multi-Level Deep Residual Learning (MDRL) network to identify malignant and benign(normal) tissues from OCT images and trains the network in 460 OCT images captured from 37 patients. The diagnostic performances are compared with different methods in the image-level and the resected patch-level. RESULTS: The MDRL system achieves the excellent diagnostic performance, with 91.2% sensitivity, 83.6% specificity, 87.5% accuracy, 85.3% PPV, and 90.2% NPV in image-level, with 0.92 AUC value. Besides, it also implements 100% sensitivity, 86.7% specificity, 93.1% accuracy, 87.5% PPV, and 100% NPV in the resected patch-level. CONCLUSION: The developed deep learning system expresses superior performance in noninvasive oral squamous cell carcinoma diagnosis, compared with traditional CNNs and a specialist.

Simultaneous Determination of Seven Pesticides and Metabolite Residues in Litchi and Longan through High-Performance Liquid Chromatography-Tandem Mass Spectrometry with Modified QuEChERS.

This study established a QuEChERS high-performance liquid chromatography/tandem triple-quadrupole mass spectrometry method for determining azoxystrobin, pyraclostrobin, picoxystrobin, difenoconazole, chlorantraniliprole, imidacloprid, and cyantraniliprole and its metabolite (IN-J9Z38) in litchi and longan, and applied this method to the real samples. The residues in samples were extracted with acetonitrile and purified with nano-ZrO2, C18, and PSA. The samples were then detected with multireactive ion monitoring and electrospray ionization in the positive ion mode and quantified using the external matrix-matched standard method. The results showed good linearities for the eight analytes in the range of 1−100 µg/L, with correlation coefficients (r2) of >0.99. The limit of quantification was 1−10 µg/kg, and the limit of detection was 0.3−3 µg/kg. Average recovery from litchi and longan was 81−99%, with the relative standard deviation of 3.5−8.4% at fortified concentrations of 1, 10, and 100 µg/kg. The developed method is simple, rapid, efficient, and sensitive. It allowed the rapid screening, monitoring, and confirming of the aforementioned seven pesticides and a metabolite in litchi and longan.

Effect of Xuebijing injection on myocardium during cardiopulmonary bypass: A prospective, randomized, double blind trial.

BACKGROUND: Cardiopulmonary bypass (CPB) is an essential procedure for maintaining the blood supply to vital organs in patients undergoing cardiac surgery. However, perioperative cardiac injury related to CPB remains a severe complication in these patients. Cardiac protection is important for patients undergoing CPB. AIM: To evaluate the potential cardioprotective efficacy of the Chinese medicine preparation Xuebijing injection (XBJ) in patients undergoing CPB. METHODS: Sixty patients undergoing cardiac surgery with CPB were randomly allocated to the XBJ and control groups (saline). XBJ was administered intravenously three times: 12 h prior to surgery, at the beginning of the surgery, and 12 h after the second injection. Cardiac function was evaluated by echocardiography 48 h after surgery. Circulating inflammation- and oxidative-stress-related markers were measured. Clinical outcomes related to intensive care unit (ICU) stay were recorded. RESULTS: Compared to control treatment, XBJ was associated with improved PaO2/FiO2 and cardiac systolic function, but reduced troponin I and creatine kinase fraction after surgery (all P < 0.05). The circulating concentrations of tumor necrosis factor-α, interleukin (IL)-1ß and IL-8 in the XBJ group were significantly lower than those in the control group (all P < 0.05), whereas the circulating concentration of IL-10 was significantly higher in the XBJ group (P < 0.05). In addition, the lengths of ICU stay and hospitalization after surgery tended to be shorter in the XBJ group than in the control group, although the differences were not significant. CONCLUSION: Perioperative administration of XBJ was associated with attenuated cardiac injury during CPB, likely via anti-inflammatory and antioxidative mechanisms.

Downregulation of macrophage migration inhibitory factor attenuates NLRP3 inflammasome mediated pyroptosis in sepsis-induced AKI.

Sepsis-induced AKI (acute kidney injury) is considered an inflammation-related disease with high mortality. LPS-induced (Lipopolysaccharide) TLR4-NFκB pathway activation plays an important role in sepsis-induced AKI. Pyroptosis closely associated with inflammation response includes inflammasome formation, caspase1 activation and GSDMD N-terminal fragment cleavage that leads to cell membrane rupture and cell death, which may be related to the pathogenesis of sepsis-induced AKI. MIF (Macrophage migration inhibitory factor), associated with inflammation response, has been proved as a biomarker of sepsis, and perhaps regulate pyroptosis in sepsis-induced AKI. In this study, we focus on investigating the mechanism of MIF promoting pyroptosis in sepsis-induced AKI. MIF and pyroptosis-related proteins were up-regulated in kidney tissue of mice with CLP (cecum ligation puncture) surgery and in LPS-injured human kidney-2 (HK-2) cells. NLRP3 was down-regulated following the suppression of MIF topoisomerase activity by ISO-1 in kidney tissue of CLP mice. Knockdown of MIF alleviated NLRP3 inflammasome mediated pyroptosis in LPS-injured HK-2 cells. Meanwhile, we noted that phosphorylation of p65 was down-regulated by knockdown of MIF. Up-regulation of NLRP3 in response to LPS stimulation could be reversed by JSH-23, an inhibitor of NFκB pathway, but MIF was not affected. In conclusion, up-regulation of MIF in sepsis-induced AKI shows a renal damaged effect that aggravates NLRP3 inflammasome mediated cell pyroptosis through promoting phosphorylation of p65. This study demonstrated a novel mechanism of MIF regulating NLRP3 inflammasome mediated pyroptosis in sepsis-induced AKI.

Iron vacancies engineering of FexC@NC hybrids toward enhanced lithium-ion storage properties.

Defect engineering have profound influence on the energy storage properties of electrode hybrids by adjusting their intrinsic electronic characteristics. For iron carbide based materials, however, the effect of defect (especially cation vacancies) toward their electrochemical performance are still unclear. Herein, the feasible and scalable synthesis of FexC@NC with 3D honeycomb-like carbon architecture and abundant Fe vacancies via template etching is reported. Such structure enable outstanding lithium-ion storage properties owing to hierarchical pores, improved intrinsic electrochemical activity, as well as the introduction of more active sites. As a result, the FexC@NC-2 presents a high reversible specific capacity of 1079 mAh g-1after 1000 cycles. Moreover, an excellent cycling stability can be achieved via maintaining a high-capacity retention (689 mAh g-1, 98.4%) over 1000 cycles at 5 A g-1. This study provides a feasible strategy for developing high-performance hybrids with hierarchical pore and rich defects structures.

Predictors of Sialocele or Salivary Fistula After Partial Superficial Parotidectomy for Benign Parotid Tumor: A Retrospective Study.

PURPOSE: Partial superficial parotid (PSP) resection is the mainstay of treatment for benign parotid tumor. Unfortunately, the post-surgical formation of sialocele or salivary fistula is a well-recognized complication of parotid surgery. The aim of this study was to determine the predictors of sialocele or salivary fistula after PSP resection for parotid benign tumor. METHODS: This retrospective cohort study includes patients who underwent PSP resection for benign parotid tumors from January 1, 2015 to December 31, 2019. The predictor variables were demographic data, systemic disease, smoking history, tumor size and type, surgical approach, and area. The outcome variables were the occurrence of sialocele or salivary fistula after PSP resection. Each possible risk factor was then examined using univariate analysis. Variables associated with sialocele or salivary fistula in the univariate analysis were then included in a multiple logistic regression model, and analyzed for possible factors related to the occurrence of sialocele or salivary fistula after partial superficial parotid resection. RESULTS: The sample was composed of 872 subjects with a mean age of 51.0 ± 8.3, and 59.5% were male. The frequency of sialocele or salivary fistula after partial superficial parotid resection was 10.4% (n = 92). Based on the multiple logistic regression model, hypertension and location of the lesion were associated with sialocoele formation. Hypertension was associated with a decreased risk for the formation of sialocele or salivary fistula (ORs = 0.6, 95% CI = [0.4,1.003], P = .051). When compared the superior lesions, anterior lesions were associated with a decreased risk for the formation of sialocele or salivary fistula (ORs = 0.32, 95% CI = [0.111,0.92], P = .034) and lesions in the middle were associated with an increased risk for sialocele or salivary fistula development (ORs = 2.315,95% CI = [1.199,4.469], P = .012). CONCLUSIONS: The incidence of sialocele or salivary fistula development was 10.4% in patients undergoing partial superficial parotidectomy in this study. Moreover, middle and anterior tumor location was shown to increase sialocele or salivary fistula risk.

Downregulation of ceramide synthase 1 promotes oral cancer through endoplasmic reticulum stress.

C18 ceramide plays an important role in the occurrence and development of oral squamous cell carcinoma. However, the function of ceramide synthase 1, a key enzyme in C18 ceramide synthesis, in oral squamous cell carcinoma is still unclear. The aim of our study was to investigate the relationship between ceramide synthase 1 and oral cancer. In this study, we found that the expression of ceramide synthase 1 was downregulated in oral cancer tissues and cell lines. In a mouse oral squamous cell carcinoma model induced by 4-nitroquinolin-1-oxide, ceramide synthase 1 knockout was associated with the severity of oral malignant transformation. Immunohistochemical studies showed significant upregulation of PCNA, MMP2, MMP9, and BCL2 expression and downregulation of BAX expression in the pathological hyperplastic area. In addition, ceramide synthase 1 knockdown promoted cell proliferation, migration, and invasion in vitro. Overexpression of CERS1 obtained the opposite effect. Ceramide synthase 1 knockdown caused endoplasmic reticulum stress and induced the VEGFA upregulation. Activating transcription factor 4 is responsible for ceramide synthase 1 knockdown caused VEGFA transcriptional upregulation. In addition, mild endoplasmic reticulum stress caused by ceramide synthase 1 knockdown could induce cisplatin resistance. Taken together, our study suggests that ceramide synthase 1 is downregulated in oral cancer and promotes the aggressiveness of oral squamous cell carcinoma and chemotherapeutic drug resistance.

Luteolin Modulates the NF-E2-Related Factor 2/Glutamate-Cysteine Ligase Pathway in Rats with Spinal Cord Injury.

Spinal cord ischemia-reperfusion injury (SCII) easily causes unalterable neurological deficits. We previously demonstrated that the flavonoid luteolin (LU) has strong antioxidant, anti-inflammatory, and other neuroprotective efficacies against SCII. In our current study, we examined the contributions of the NF-E2-related factor 2 (Nrf2)/glutamate-cysteine ligase (GCL) pathway to LU-mediated neuroprotection in the transient abdominal aorta occlusion rat model of SCII. Rats were divided into four groups: Sham surgery, SCII alone, SCII plus LU pretreatment (SCII + LU), and SCII plus cotreatment with LU and the Nrf2 inhibitor ML385 (SCII + LU + ML385). The Basso-Beattie-Bresnahan (BBB) scale was used to assess neurological function, hematoxylin and eosin staining to evaluate pathological change to the spinal cord, and enzyme-linked immunosorbent assay to measure tissue markers of oxidative stress and inflammation induced by SCII. Mitochondrial injury and apoptosis were examined by flow cytometry and expression levels of Nrf2, GCL catalytic subunit (GCLc), and GCL modifier subunit (GCLm) by real-time quantitative polymerase chain reaction. LU pretreatment significantly enhanced recovery of motor function as evidenced by the BBB score and attenuated the pathological damage. Furthermore, LU effectively enhanced the antioxidative activity, alleviated mitochondrial swelling, decreased the expression levels of several proinflammatory cytokines after SCII, and significantly upregulated Nrf2, GCLc, and GCLm expression levels. Cotreatment with ML385 reversed all these protective effects of LU except the anti-inflammatory response. Collectively, these findings indicate that the neuroprotective efficacy of LU depends on suppression of oxidative stress and preservation of mitochondrial function through signaling pathways involving Nrf2 activation and downstream gene expression.

Co-existence of lung carcinoma metastasis and enchondroma in the femur of a patient with Ollier disease.

Tumour-to-tumour metastasis is very unusual and has been defined as a tumour metastasis into another histologically different tumour. It is extremely rare in bone. We report a case of lung squamous cell carcinoma metastasized to an enchondroma in the femur of a patient with Ollier disease. A 60-year-old female had a history of a poorly differentiated squamous cell carcinoma of the lung. She underwent a video-assisted thoracoscopic lobectomy, and a follow-up MRI scan showed three lesions in the left distal femur and proximal tibia, which were initially interpreted as metastasis on radiology. Resection of the left proximal tibial lesion was performed, and the pathological findings were consistent with enchondroma with no evidence of metastasis. Subsequent curettage of lesions in the distal left femur revealed metastatic poorly differentiated carcinoma with foci of hyaline cartilage, which was most consistent with metastatic carcinoma in a pre-existing enchondroma. The MRI films were re-reviewed. Characteristic MRI features of enchondroma were found in the lesion in the left proximal tibia and one of the lesions in the left distal femur, while the features of the other lesion in the left distal femur included cortical destruction and extensive oedema in surrounding soft tissue, which were consistent with a malignant tumour. In addition, the enchondroma in the lateral condyle showed blurring and irregular inner margin and adjacent bone oedema, which likely represents a co-existing metastatic tumour and enchondroma. The difference in lineage was confirmed by immunohistochemistry. The final diagnosis was metastatic poorly differentiated carcinoma of the lung into a co-existent enchondroma. The diagnosis can be challenging and could be easily overlooked both radiologically and histologically. Thorough clinical and radiological information is critical for the diagnosis, and despite a very unusual event, awareness of the tumour-to-tumour metastasis phenomenon can avoid an inaccurate diagnosis by the pathologist, therefore preventing inappropriate clinical intervention.

Ac2-26 Alleviates Brain Injury after Cardiac Arrest and Cardiopulmonary Resuscitation in Rats via the eNOS Pathway.

BACKGROUND: Brain injury is the leading cause of death following cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). Ac2-26 and endothelial nitric oxide synthase (eNOS) have been shown to reduce neuroinflammation. This study is aimed at determining the mechanism by which Ac2-26 protects against inflammation during brain injury following CA and CPR. METHODS: Sixty-four rats were randomized into sham, saline, Ac2-26, and Ac2-26+L-NIO (endothelial nitric oxide synthase (eNOS) inhibitor) groups. Rats received Ac2-26, Ac2-26+L-NIO, or saline after CPR. Neurologic function was assessed at baseline, 24, and 72 hours after CPR. At 72 hours after resuscitation, serum and brain tissues were collected. RESULTS: Blood-brain barrier (BBB) permeability increased, and the number of surviving neurons and neurological function decreased in the saline group compared to the sham group. Anti-inflammatory and proinflammatory factors, neuron-specific enolase (NSE) levels, and the expression of eNOS, phosphorylated (p)-eNOS, inducible nitric oxide synthase (iNOS), and oxidative stress-related factors in the three CA groups significantly increased (P < 0.05). BBB permeability decreased, and the number of surviving neurons and neurological function increased in the Ac2-26 group compared to the saline group (P < 0.05). Ac2-26 increased anti-inflammatory and reduced proinflammatory markers, raised NSE levels, increased the expression of eNOS and p-eNOS, and reduced the expression of iNOS and oxidative stress-related factors compared to the saline group (P < 0.05). The effect of Ac2-26 on brain injury was reversed by L-NIO (P < 0.05). CONCLUSIONS: Ac2-26 reduced brain injury after CPR by inhibiting oxidative stress and neuroinflammation and protecting the BBB. The therapeutic effect of Ac2-26 on brain injury was largely dependent on the eNOS pathway.

Astaxanthin alleviates spinal cord ischemia-reperfusion injury via activation of PI3K/Akt/GSK-3ß pathway in rats.

BACKGROUND: Ischemia-reperfusion injury of the spinal cord (SCII) often leads to unalterable neurological deficits, which may be associated with apoptosis induced by oxidative stress and inflammation. Astaxanthin (AST) is a strong antioxidant and anti-inflammatory agent with multitarget neuroprotective effects. This study aimed to investigate the potential therapeutic effects of AST for SCII and the molecular mechanism. METHODS: Rat models of SCII with abdominal aortic occlusion for 40 min were carried out to investigate the effects of AST on the recovery of SCII. Tarlov's scores were used to assess the neuronal function; HE and TUNEL staining were used to observe the pathological morphology of lesions. Neuron oxidative stress and inflammation were measured using commercial detection kits. Flow cytometry was conducted to assess the mitochondrial swelling degree. Besides, Western blot assay was used to detect the expression of PI3K/Akt/GSK-3ß pathway-related proteins, as well as NOX2 and NLRP3 proteins. RESULTS: The results demonstrated that AST pretreatment promoted the hind limb motor function recovery and alleviated the pathological damage induced by SCII. Moreover, AST significantly enhanced the antioxidative stress response and attenuated mitochondrial swelling. However, AST pretreatment hardly inhibited the levels of proinflammatory cytokines after SCII. Most importantly, AST activated p-Akt and p-GSK-3ß expression levels. Meanwhile, cotreatment with LY294002 (a PI3K inhibitor) was found to abolish the above protective effects observed with the AST pretreatment. CONCLUSION: Overall, these results suggest that AST pretreatment not only mitigates pathological tissue damage but also effectively improves neural functional recovery following SCII, primarily by alleviating oxidative stress but not inhibiting inflammation. A possible underlying molecular mechanism of AST may be mainly attributed to the activation of PI3K/Akt/GSK-3ß pathway.

Endothelial colony-forming cells reduced the lung injury induced by cardiopulmonary bypass in rats.

BACKGROUND: Cardiopulmonary bypass (CPB) results in severe lung injury via inflammation and endothelial injury. The aim of this study was to evaluate the effect of endothelial colony-forming cells (ECFCs) on lung injury in rats subjected to CPB. METHODS: Thirty-two rats were randomized into the sham, CPB, CPB/ECFC and CPB/ECFC/L-NIO groups. The rats in the sham group received anaesthesia, and the rats in the other groups received CPB. The rats also received PBS, ECFCs and L-NIO-pre-treated ECFCs. After 24 h of CPB, pulmonary capillary permeability, including the PaO2/FiO2 ratio, protein levels in bronchoalveolar lavage fluid (BALF) and lung tissue wet/dry weight were evaluated. The cell numbers and cytokines in BALF and peripheral blood were tested. Endothelial injury, lung histological injury and apoptosis were assessed. The oxidative stress response and apoptosis-related proteins were analysed. RESULTS: After CPB, all the data deteriorated compared with those obtained in the S group (sham vs CPB vs CPB/ECFC vs CPB/ECFC/L-NIO: histological score 1.62 ± 0.51 vs 5.37 ± 0.91 vs 3.37 ± 0.89 vs 4.37 ± 0.74; PaO2/FiO2 389 ± 12 vs 233 ± 36 vs 338 ± 28 vs 287 ± 30; wet/dry weight 3.11 ± 0.32 vs 6.71 ± 0.73 vs 4.66 ± 0.55 vs 5.52 ± 0.57; protein levels in BALF: 134 ± 22 vs 442 ± 99 vs 225 ± 41 vs 337 ± 53, all P < 0.05). Compared to the CPB treatment, ECFCs significantly improved pulmonary capillary permeability and PaO2/FiO2. Similarly, ECFCs also decreased the inflammatory cell number and pro-inflammatory factors in BALF and peripheral blood, as well as the oxidative stress response in the lung tissue. ECFCs reduced the lung histological injury score and apoptosis and regulated apoptosis-related proteins in the lung tissue. Compared with the CPB/ECFC group, all the indicators were partly reversed by the L-NIO. CONCLUSIONS: ECFCs significantly reduced lung injury induced by inflammation after CPB.

POM121 overexpression is related to a poor prognosis in colorectal cancer.

Background: Nuclear pore membrane protein 121 (POM121) plays a crucial role in nucleocytoplasmic transport, but its significance in tumorigenesis and the progression of colorectal cancer (CRC) remains unknown. The aim of this study was to evaluate the relationship between POM121 and CRC.Methods: POM121 expression in colorectal tissues was analyzed at both the gene and protein levels. We investigated the connection between POM121 expression and clinicopathological features, as well as overall survival. A gene set enrichment analysis (GSEA) was performed, and a protein-protein interaction (PPI) network was constructed to determine the mechanism of POM121 in CRC.Results: CRC tissues displayed a striking increase in POM121 expression compared with colonitis and pericarcinomatous mucosa tissues (66.61% vs 24.36% vs 24.11%, respectively, p < 0.0167). POM121 overexpression was significantly associated with lymph node metastasis, distant metastasis, TNM stage, venous invasion, perineural invasion, preoperative CEA and CA19-9 levels, and Ki67 expression. CRC patients with high POM121 levels tended to have poor overall survival rates. POM121 may participate in the regulation of the cell cycle and DNA repair in CRC.Conclusions: Our results suggest that POM121 has the potential to serve as a novel prognostic biomarker in CRC patients.

4.1B suppresses cancer cell proliferation by binding to EGFR P13 region of intracellular juxtamembrane segment.

BACKGROUND: Gastric cancer (GC) has high incidence and mortality worldwide. However, the underlying mechanisms that regulate gastric carcinogenesis are largely undefined. 4.1B is an adaptor protein found at the interface of membrane and the cytoskeleton. Previous studies demonstrated that 4.1B serves as tumor suppressor. RESULTS: We showed that 4.1B expression was decreased or lost in most GC patients. The expression pattern of it was tightly correlated with tumor size, TNM stage and overall survival (OS). We further showed that 4.1B inhibited the proliferation of two GC cell lines, MGC-803 and MKN-45, by impeding the EGFR/MAPK/ERK1/2 and PI3K/AKT pathways. A similar phenotype was also observed in immortalized mouse embryonic fibroblasts (MEF) derived from wild type (WT) and 4.1B knock-out (BKO) mice. Additionally, immunofluorescence (IF) staining and Co-IP showed that protein 4.1B bound to EGFR. Furthermore, the FERM domain of 4.1B interacted with EGFR through the initial 13 amino acids (P13) of the intracellular juxtamembrane (JM) segment of EGFR. The binding of 4.1B to EGFR inhibited dimerization and autophosphorylation of EGFR. CONCLUSION: Our present work revealed that 4.1B plays important regulatory roles in the proliferation of GC cells by binding to EGFR and inhibiting EGFR function through an EGFR/MAPK/ERK1/2 pathway. Our results provide novel insight into the mechanism of the development and progression of GC.

[Clavicle fracture after radical neck dissection of mouth floor carcinoma misdiagnosed as cervical metastasis: a case report].

Clavicle fracture, a very rare delayed complication following radical neck dissection of oral carcinoma, is normally ignored by oral and maxillofacial surgeons. We report and analyze a male patient with clavicle fracture after primary extended excision and bilateral radical neck dissection. This case was misdiagnosed as cervical metastasis.

Oral Glucosamine Hydrochloride Combined With Hyaluronate Sodium Intra-Articular Injection for Temporomandibular Joint Osteoarthritis: A Double-Blind Randomized Controlled Trial.

PURPOSE: Temporomandibular joint (TMJ) disorders occur in many people and osteoarthritis (OA) is a severe form of this disease. Glucosamine has been used to treat OA of the large joints for many years and has been proved effective. A double-blinded randomized controlled trial was designed to investigate the effectiveness and safety of oral glucosamine hydrochloride pills combined with hyaluronate sodium intra-articular injection in TMJ OA. PATIENTS AND METHODS: One hundred forty-four participants with TMJ OA were randomized to 4 hyaluronate sodium injections and oral glucosamine hydrochloride (1.44 g/day) for 3 months (group A) or 4 hyaluronate sodium injections and oral placebo for 3 months (group B). All participants were followed for 1 year. Eighteen participants were lost to follow-up. RESULTS: The intention-to-treat analysis showed that group A had similar maximal interincisal mouth opening and pain intensity during TMJ function at months 1 and 6 (P > .05). However, during long-term follow-up, group A had significantly greater maximal interincisal mouth opening compared with group B at month 12 (41.5 vs 37.9 mm; P < .001). For pain intensity, group A showed obviously lower visual analog scale scores than group B at month 6 (20.6 vs 29.2 mm; P = .007) and month 12 (17.4 vs 28.6 mm; P = .001). Twenty-four participants had gastrointestinal tract side effects, fatigue, and rash. Of these, 23 had slight side effects that were not correlated with glucosamine. There was no significant difference between the 2 groups (P > .05). CONCLUSION: The results of this study suggest that, compared with hyaluronate sodium injection alone, glucosamine hydrochloride pills added to hyaluronate sodium injection had no meaningful effect on TMJ OA in the short-term but did relieve the pain caused by TMJ OA and improved TMJ functions in the long-term.

[Determination of myclobutanil and difenoconazole residues in pollen and honey of litchi by high performance liquid chromatography-tandem mass spectrometry].

An effective method was developed for the determination of two major fungicides including myclobutanil and difenoconazole residues in pollen and honey of litchi by modified QuEChERS-high performance liquid chromatography-tandem mass spectrometry (HPLC-MS/MS). The pollen and honey samples were all extracted by acetonitrile, the pollen samples were cleaned-up by 0.9 g anhydrous magnesium sulfate (MgSO4), 0.15 g primary secondary amine (PSA) and 0.15 g C18; the honey samples were cleaned-up by 0.9 g MgSO4 and 0.15 g PSA. The 0.1% (v/v) formic acid aqueous solution-acetonitrile (25:75, v/v) were used as the mobile phases. The extracts were separated on a Poroshell-120 EC-C18 chromatographic column, the positive electrospray ion (ESI+) source and selected ion monitoring (SIM) mode were used. The analytes were quantified by the matrix matching standard solutions. The matrix matched standard solutions of myclobutanil and difenoconazole showed good linearities in the range of 1-100 µg/L, and the correlation coefficients (r2) were all above 0.9990. The limits of detection (LODs) of myclobutanil and difenoconazole were 0.25 µg/kg and 0.50 µg/kg, respectively. The limits of quantification (LOQs) of myclobutanil and difenoconazole were 0.83 µg/kg and 1.7 µg/kg, respectively. The average recoveries of myclobutanil and difenoconazole in pollen and honey samples were 87.0%-95.2% and 90.1%-96.4% with the relative standard deviations of 1.2%-3.6% and 0.7%-4.1%, respectively. The method is quick, easy and sensitive, and it is suitable for the rapid determination and trace analysis of myclobutanil and difenoconazole in pollens and honeys of litchi. The method can provide data support for the exposure risk assessment of bees and other pollination insects.