A modified Blumgart anastomosis with a simple and practicable procedure after laparoscopic pancreaticoduodenectomy: our center's experience.

BACKGROUND: Laparoscopic pancreaticoduodenectomy(LPD) has become the goal of lots of minimally invasive surgical centers in recent years. Postoperative pancreatic fistula(POPF) is still the barrier to attaining the above goal. Thus, improving anastomosis techniques to reduce the rate of POPF has been a hotspot of surgery. Blumgart pancreaticojejunostomy is considered one of the best anastomosis procedures, with low rates of POPF. However, the original Blumgart pancreaticojejunostomy method is not easy for laparoscopic operation. In consequence, we modified a Blumgart pancreaticojejunostomy technique with a simple and practicable procedure and applied to LPD. METHODS: We collected and retrospectively analyzed the perioperative clinical data of patients who underwent modified Blumgart anastomosis from February 2017 to September 2022. The above patients included 53 cases in open pancreaticojejunostomy(OPD) and 58 cases in LPD. After propensity score matching, 44 cases were included for comparison in each group. RESULTS: After propensity score matching, the average time for pancreaticojejunostomy was about 30 min in the LPD group. The Clinically relevant POPF(CR-POPF) rate was 9.1%. The length of postoperative hospitalization was 13.1 days. Compared with the OPD group, The CR-POPF rate in the LPD group are not significant differences. But the postoperative length of hospital stay was significantly shorter in the LPD group. Besides, there were no other severely postoperative complications between two groups. CONCLUSION: The modified Blumgart anastomosis technique applied to LPD in our Center not only has simple and convenient properties but also low rate of CR-POPF. And this method may be a good choice for surgeons to begin to carry out LPD.

Spontaneous intracapsular hemorrhage of a giant hepatic cavernous hemangioma: a rare case report and literature review.

BACKGROUND: Hepatic cavernous hemangioma is the most common type of benign liver tumor. Although ruptures and hemorrhages of hepatic hemangioma are rare complications, they are associated with high mortality. Most practitioners only pay more attention to abdominal hemorrhages caused by the rupture of hepatic hemangiomas. However, spontaneous intracapsular hemorrhages can often be neglected and poorly understood. CASE PRESENTATION: A 65-year-old man was referred to our institution with right upper quadrant pain, which had occurred suddenly and without a history of recent trauma. The blood test results were normal. Magnetic resonance imaging (MRI) of the abdomen showed a cystic mass in the right liver lobe. Considering the possibility of hepatic cystadenoma with hemorrhage, the patient underwent a right hepatic lobectomy. The pathological findings unexpectedly revealed intratumoral hemorrhage of hepatic hemangioma. The patient recovered well and was discharged eight days after surgery. CONCLUSIONS: Intracapsular hemorrhage of hepatic cavernous hemangioma is challenging to diagnose and has a high potential risk of rupture. MRI is beneficial for diagnosing subacute internal hemorrhage cases, and it is recommended to undergo surgery for patients with a definitive diagnosis.

Zinc mediates the SREBP-SCD axis to regulate lipid metabolism in Caenorhabditis elegans.

Maintenance of lipid homeostasis is crucial for cells in response to lipid requirements or surplus. The SREBP transcription factors play essential roles in regulating lipid metabolism and are associated with many metabolic diseases. However, SREBP regulation of lipid metabolism is still not completely understood. Here, we showed that reduction of SBP-1, the only homolog of SREBPs in Caenorhabditis elegans, surprisingly led to a high level of zinc. On the contrary, zinc reduction by mutation of sur-7, encoding a member of the cation diffusion facilitator (CDF) family, restored the fat accumulation and fatty acid profile of the sbp-1(ep79) mutant. Zinc reduction resulted in iron overload, which thereby directly activated the conversion activity of stearoyl-CoA desaturase (SCD), a main target of SREBP, to promote lipid biosynthesis and accumulation. However, zinc reduction reversely repressed SBP-1 nuclear translocation and further downregulated the transcription expression of SCD for compensation. Collectively, we revealed zinc-mediated regulation of the SREBP-SCD axis in lipid metabolism, distinct from the negative regulation of SREBP-1 or SREBP-2 by phosphatidylcholine or cholesterol, respectively, thereby providing novel insights into the regulation of lipid homeostasis.

MicroRNA-520c-3p inhibits hepatocellular carcinoma cell proliferation and invasion through induction of cell apoptosis by targeting glypican-3.

AIM: Glypican-3 (GPC3) is a membrane-associated heparan sulfate proteoglycan involved in regulation of cell proliferation, cell survival, cell migration and differentiation process. MicroRNAs (miRNAs) are single-stranded, non-coding functional RNAs that are important in many biological processes. GPC3 and miRNAs have been found to play essential roles in the development and progression of hepatocellular carcinoma (HCC). However, little information about the relationship between GPC3 and miRNAs is available nowadays. Therefore, this study aims to examine the relationship between GPC3 and miRNAs. METHODS: Dual-luciferase reporter assay was used to validate the direct target of GPC3. Fluorescence quantitative PCR and Western blotting were used to examined the gene expression at mRNA and protein levels. Cell apoptosis was evaluated by flow cytometric analysis and Annexin V-FITC staining. Invasion of cells was evaluated by Transwell matrigel assay. RESULTS: The results showed that miR-520c-3p could specifically target GPC3 in HCC cells. GPC3 protein levels decreased with unchanged transcription efficiency after miRNA transfection, and there was negative correlation of miR-520c-3p expression in HCC in relate to GPC3 protein levels. Moreover, miR-520c-3p not only induced HCC cell apoptosis, but also inhibited the growth and invasion of the cells. Interestingly, overexpression of GPC3 could effectively reverse apoptosis induced by miR-520c-3p transfection in HCC. CONCLUSIONS: Taken together, these results supported that miR-520c-3p may decrease GPC3 protein levels to inhibit proliferation of HCC cells. Therefore, GPC3 could be a new target for genetic diagnosis and treatment of HCC.

REEP3 is a potential diagnostic and prognostic biomarker correlated with immune infiltration in pancreatic cancer.

Receptor Expression-Enhancing Protein 3 (REEP3) serves as a pivotal enzyme crucial for endoplasmic reticulum (ER) clearance during mitosis and is implicated in the advancement of diverse malignancies. Nonetheless, the biological role and mechanisms of REEP3 in pancreatic cancer patients, along with its interplay with immune infiltration, remain inadequately elucidated. In this study, we initially analyzed the differential expression of REEP3 between pancreatic cancer tissues and normal pancreas tissues using the Cancer Genome Atlas (TCGA), GTEx and Gene Expression Omnibus (GEO) databases. Subsequently, we utilized Kaplan-Meier analysis, Cox regression and ROC curve to determine the predictive value of REEP3 for the clinical outcomes of pancreatic cancer patients. Functional enrichment analyses, including Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Set Enrichment Analysis (GSEA), were conducted to explore the potential signaling pathways and biological functions associated with pancreatic cancer. Furthermore, we investigated the PPI network, miRNA, RBP and transcription factor interactions of REEP3 using databases such as GeneMania, STRING, StarBase, KnockTK, ENCODE, Jaspar and hTFtarget. Lastly, the "ssGSEA" algorithm and TIMER database were employed to investigate the correlation between REEP3 expression and immune infiltration as well as immune checkpoints. The expression of REEP3 in pancreatic cancer showed a significantly higher level compared to that in normal tissues. ROC curve analysis indicated that REEP3 holds substantial diagnostic potential for pancreatic cancer patients. Elevated REEP3 expression correlated with unfavorable outcomes in terms of both overall survival and relapse-free survival, establishing it as a notable adverse prognostic marker in pancreatic cancer. Moreover, both univariate and multivariate Cox regression analyses demonstrated that REEP3 maintained an independent association with overall survival. Functional enrichment analyses revealed pathways significantly linked to REEP3, including cytoplasmic translation, wound healing, viral processes, regulation of cellular component size and actin filament organization. Additionally, REEP3 expression displayed a significant positive correlation with CD8+ T cells, B cells, natural killer cells, dendritic cells and macrophages. REEP3 is a potential diagnostic, prognostic marker and immunotherapeutic target for pancreatic cancer.

Hydraulic properties and drought response of a tropical bamboo (Cephalostachyum pergracile).

Bamboo plants are an essential component of tropical ecosystems, yet their vulnerability to climate extremes, such as drought, is poorly understood due to limited knowledge of their hydraulic properties. Cephalostachyum pergracile, a commonly used tropical bamboo species, exhibited a substantially higher mortality rate than other co-occurring bamboos during a severe drought event in 2019, but the underlying mechanisms remain unclear. This study investigated the leaf and stem hydraulic traits related to drought responses, including leaf-stem embolism resistance (P50leaf; P50stem) estimated using optical and X-ray microtomography methods, leaf pressure-volume and water-releasing curves. Additionally, we investigated the seasonal water potentials, native embolism level (PLC) and xylem water source using stable isotope. We found that C. pergracile exhibited strong resistance to embolism, showing low P50leaf, P50stem, and turgor loss point, despite its rapid leaf water loss. Interestingly, its leaves displayed greater resistance to embolism than its stem, suggesting a lack of effective hydraulic vulnerability segmentation (HVS) to protect the stem from excessive xylem tension. During the dry season, approximately 49% of the water was absorbed from the upper 20-cm-deep soil layer. Consequently, significant diurnal variation in leaf water potentials and an increase in midday PLC from 5.87 ± 2.33% in the wet season to 12.87 ± 4.09% in the dry season were observed. In summary, this study demonstrated that the rapid leaf water loss, high reliance on surface water, and a lack of effective HVS in C. pergracile accelerated water depletion and increased xylem embolism even in the typical dry season, which may explain its high mortality rate during extreme drought events in 2019.

Knockdown of GPC3 inhibits the proliferation of Huh7 hepatocellular carcinoma cells through down-regulation of YAP.

Glypican-3 (GPC3), a membrane-associated heparan sulfate proteoglycan, is frequently upregulated in hepatocellular carcinoma (HCC). Yes-associated protein (YAP) is also found over-expressed in HCC and has been identified as a key effector molecule in Hippo pathway, which could control the organ size in animals through the regulation of cell proliferation and apoptosis and plays an important role in the development of malignant tumors. Studies have reported that GPC3 and YAP might collaborate to regulate the development of HCC. To elucidate the role of GPC3 in the development of HCC and its relationship with YAP, siRNA technique was employed to knock down GPC3 in Huh7 HCC cells. Moreover, recombinant human YAP-1 was used to examine the effects of GPC3 on Huh7 cells. The results of flow cytometric analysis and Annexin-V-FLUOS apoptosis assay showed that knockdown of GPC3-induced apoptosis in Huh7 cells, resulting in inhibition of cell proliferation as examined by EdU incorporation assay, migration, and invasion. GPC3 knockdown also suppressed the expression of YAP in mRNA and protein levels, as examined by fluorescence quantitative PCR and Western blot analysis. Moreover, addition of recombinant human YAP-1 effectively rescued the cells from apoptosis triggered by GPC3 knockdown. Taken together, our findings suggest that GPC3 regulates HCC cell proliferation with the involvement of Hippo pathway.

Adjuvant activity of Sargassum pallidum polysaccharides against combined Newcastle disease, infectious bronchitis and avian influenza inactivated vaccines.

This study evaluates the effects of Sargassum pallidum polysaccharides (SPP) on the immune responses in a chicken model. The adjuvanticity of Sargassum pallidum polysaccharides in Newcastle disease (ND), infectious bronchitis (IB) and avian influenza (AI) was investigated by examining the antibody titers and lymphocyte proliferation following immunization in chickens. The chickens were administrated combined ND, IB and AI inactivated vaccines containing SPP at 10, 30 and 50 mg/mL, using an oil adjuvant vaccine as a control. The ND, IB and AI antibody titers and the lymphocyte proliferation were enhanced at 30 mg/mL SPP. In conclusion, an appropriate dose of SPP may be a safe and efficacious immune stimulator candidate that is suitable for vaccines to produce early and persistent prophylaxis.

[Effect of Saikosaponins-d on reversing malignant phenotype of HepG2 cells in vitro].

OBJECTIVE: To observe the effect of SSd on reversing the malignant phenotype of HepG2 cells and to investigate its mechanism in order to prove that SSd is a new choice to prevent and treat HCC. METHODS: HepG2 cells were cultured and treated by different concentration (0 mg/L, 2.5 mg/L, 5.0 mg/L, 10.0 mg/L and 20.0 mg/L) of SSd for 24 h, and treated by 10 mg/L of SSd for 0 h, 6 h, 12 h, 24 h, 48 h and 72h respectively. The cell inhibition rates were measured by MTT assay. Then cells were treated by 10 mg/L SSd for 48 hr in experimental group and treated by no SSd as a control, their morphological changes were observed by contrast phase microscope. The concentrations of ALB and AFP in clear supernatant liquid of cells were detected by radio-immunity and chemiluminescence. The cell migration rates were observed by transwell method, the relative expression levels of p27 mRNA were measured by RT-PCR. RESULTS: The inhibitive effect of 10 mg/L SSd was the most significant among different concentrations ( F = 265.06, P less than 0.01). The shape of HepG2 from experimental group turned into small and round, and their volume ratios of nucleus to plasma decreased. ALB in supernatant liquid of HepG2 was higher ( t = 7.83, P less than 0.05, and its AFP was lower ( t = -10.72, P less than 0.01) as compared to control group. Cells migrated were fewer and p27 mRNA expression of HepG2 was higher in experimental group than that in control group (t = 22.00, P less than 0.05). CONCLUSION: SSd could reverse the malignant phenotype of HepG2 cells. It was suggested that the up-regulation of p27 mRNA expression play an important role in the differentiation of HepG2 cells treated by SSd.

PBK phosphorylates MSL1 to elicit epigenetic modulation of CD276 in nasopharyngeal carcinoma.

CD276 (also known as B7-H3, an immune checkpoint molecule) is aberrantly overexpressed in many cancers. However, the upregulation mechanism and in particular, whether oncogenic signaling has a role, is unclear. Here we demonstrate that a pro-oncogenic kinase PBK, the expression of which is associated with immune infiltration in nasopharyngeal carcinoma (NPC), stimulates the expression of CD276 epigenetically. Mechanistically, PBK phosphorylates MSL1 and enhances the interaction between MSL1 and MSL2, MSL3, and KAT8, the components of the MSL complex. As a consequence, PBK promotes the enrichment of MSL complex on CD276 promoter, leading to the increased histone H4 K16 acetylation and the activation of CD276 transcription. In addition, we show that CD276 is highly upregulated and associated with immune infiltrating levels in NPC. Collectively, our findings describe a novel PBK/MSL1/CD276 signaling axis, which may play an important role in immune evasion of NPC and may be targeted for cancer immunotherapy.

FSCN1 Promotes Radiation Resistance in Patients With PIK3CA Gene Alteration.

Radiotherapy is one of the standard treatments for cervical cancer and head and neck cancer. However, the clinical efficacy of this treatment is limited by radioresistance. The discovery of effective prognostic biomarkers and the identification of new therapeutic targets have helped to overcome the problem of radioresistance. In this study, we show that in the context of PIK3CA mutation or amplification, high expression of fascin actin-bundling protein 1 (FSCN1) (using the median as the cut-off value) is associated with poor prognosis and radiotherapy response in cancer patients. Silencing FSCN1 enhances radiosensitivity and promotes apoptosis in cancer cells with PIK3CA alterations, and this process may be associated with the downregulation of YWHAZ. These results reveal that FSCN1 may be a key regulator of radioresistance and could be a potential target for improving radiotherapy efficacy in cervical cancer and head and neck cancer patients with PIK3CA alterations.

Identify potential clinical significance of long noncoding RNA forkhead box P4 antisense RNA 1 in patients with early stage pancreatic ductal adenocarcinoma.

Previous studies have shown that forkhead box P4 antisense RNA 1 (FOXP4-AS1) is dysregulated in tumor tissues and can serve as a prognostic indicator for multiple cancers. However, the clinical significance of FOXP4-AS1 in pancreatic ductal adenocarcinoma (PDAC) remains unclear. The goal of this study is to recognize the possible clinical significance of long noncoding RNA FOXP4-AS1 in patients with early stage PDAC. A total of 112 patients from The Cancer Genome Atlas (TCGA) PDAC cohort, receiving RNA sequencing, were involved in the study. Survival analysis, functional mechanism, and potential small molecule drugs of target therapy of FOXP4-AS1 were performed in this study. Survival analysis in TCGA PDAC cohort suggested that patients with high FOXP4-AS1 expression had significantly augmented possibility of death than in PDAC patients with lower FOXP4-AS1 expression (adjusted P = .008; adjusted HR = 2.143, 95% CI = 1.221-3.760). In this study, a genome-wide RNA sequencing dataset was used to identify 927 genes co-expressing with FOXP4-AS1 in PDAC tumor tissues. A total of 676 differentially expressed genes were identified between different FOXP4-AS1 expression groups. Functional enrichment analysis of these genes and gene set enrichment analysis for PDAC genome-wide RNA sequencing dataset was done. We have found that FOXP4-AS1 may function in PDAC by participating in biological processes and pathways including oxidative phosphorylation, tricarboxylic acid cycle, classical tumor-related pathways such as NF-kappaB as well as Janus kinase/signal transducers in addition to activators of transcription, cell proliferation, and adhesion. In addition, we also screened two potential targeted therapeutic small molecule drugs (dimenhydrinate and metanephrine) for FOXP4-AS1 in PDAC. In conclusion, our present study demonstrated that higher expression of FOXP4-AS1 in PDAC tumor tissues were related with an inferior medical outcome. Through multiple genome-wide approaches, we identified the potential molecular mechanisms of FOXP4-AS1 in PDAC and two targeted therapeutic drugs for it.

Theoretical study of H-atom abstraction reactions from CH3CH2OCH2CH3, CHF2CF2OCH2CF3 and CF3CH2OCH3 by NO3 radical & subsequent degradation.

The nocturnal reactions of CH3CH2OCH2CH3, CHF2CF2OCH2CF3 and CF3CH2OCH3 initiated by NO3 radicals are important sources of alkyl radicals and nitric acids. In this paper, the thermodynamics and kinetics of CH3CH2OCH2CH3, CHF2CF2OCH2CF3 and CF3CH2OCH3 induced by NO3 radical in gas phase are studied in detail by BHandHLYP method combined with 6-311G(d,p) basis set, and the single point correction is calculated by relatively accurate CCSD(T) method. In the temperature range of 200-400 K, the rate constants of title reactions are fitted to the three-parameter Arrhenius formula: k1 = 1.13 × 10-40T9.24exp(1675.99/T) k2 = 2.23 × 10-23T2.81exp(-4476.24/T) k3 = 5.63 × 1043T-19.20exp(-9344.12/T) All the rate constants calculated by the canonical variational transition state theory and the small curvature tunneling are basically consistent with the limited experimental data. By comparing the reaction rate constants of ethyl ether and its isomer methyl propyl ether with NO3 radical at 293 ±â€¯2 K, the higher the symmetry is, the faster the reaction rate of ether is. Thermodynamic calculations and kinetic data of the title reactions indicate that the H-abstraction reactions at the -OCH2- sites are the main reaction pathways. The thermodynamic and kinetic data of the reaction CH3CH2OCH2CH3, CHF2CF2OCH2CF3 with NO3 radical, showing that the reaction activity could be reduced due to the addition of fluorine atoms, which is further verified by the enthalpies, Gibbs free energies of the title reactions and C-H bond dissociation energies of the CH3CH2OCH2CH3, CHF2CF2OCH2CF3 and CF3CH2OCH3 molecules. The reaction thermodynamics and kinetics are determined, and the formation mechanisms of the products are proposed, which are crucial to determine the influence of CH3CH2OCH2CH3, CHF2CF2OCH2CF3 and CF3CH2OCH3 on air quality, as well as its atmospheric lifetime and durability. The atmospheric lifetimes of CH3CH2OCH2CH3, CHF2CF2OCH2CF3 and CF3CH2OCH3 are evaluated in the NO3-concentration range of 5 × 108-2 × 109 molecule cm-3 to fully consider the effects of different regions on their nocturnal migration. The radiation efficiency and global warming potentials (GWPs) have been reported. The products of title reaction CH3CH2OCHCH3, CF3CHOCF2CHF2 and CF3CHOCH3 are further oxidized into organic nitrates in the presence of O2 and NO. Organic nitrites can be isomerized into organic nitrates or degraded to form CH3C(O•)HOCH2CH3, CF3C(O•)HOCF2CHF2 and CH3C(O•)HOCF3 alkoxy radicals and NO2. This work provides deep insight into the night migration and transformation mechanism of the three ethers.

A total laparoscopic treatment strategy for Amyand's hernia complicated with appendicitis: A case report.

INTRODUCTION: The presence of a vermiform appendix in an inguinal hernia sac is known as Amyand's hernia. It is even rarer with complicated appendicitis. Formerly it was treated via an open groin approach; recently there are new trends involving the use of laparoscopy for reduction and management of appendix. Conversely the role of laparoscopy in the following hernia repair was less discussed, with no standard care. We reported a case of Amyand's hernia complicated with appendix which was managed via a total laparoscopic strategy. PRESENTATION OF CASE: A 49-year-old male presented with right groin mass with progressive pain for 3 days. Physical exams revealed incarcerated right inguinal hernia. Amyand's hernia with acute appendicitis was diagnosed preoperatively via computed tomography (CT). Emergent diagnostic laparoscopy was performed. Appendix was reduced, with appendectomy justified for signs of appendicitis. An interval total extraperitoneal (TEP) hernioplasty was performed 3 month later, with no adverse events postoperatively. DISCUSSION: In virtue of previous literature, we proposed a total laparoscopic strategy for Amyand's hernia which consists of transabdominal diagnostic laparoscopy, management of appendix, and either immediate or elective laparoscopic hernioplasty, based on status of appendix. CONCLUSION: This laparoscopic treatment strategy is feasible for Amyand's hernia, with minimized risk of surgical site infection (SSI), fair recovery and cosmesis.

A mixture of citrus polymethoxyflavones, green tea polyphenols and lychee extracts attenuates adipogenesis in 3T3-L1 adipocytes and obesity-induced adipose inflammation in mice.

Adipocyte-macrophage interaction in obesity can cause adipose tissue inflammation and contribute to insulin resistance. Here, we investigated the effect of SlimTrym®-a formulated product containing citrus polymethoxyflavones (PMFs), green tea extract, and lychee polyphenols-on 3T3-L1 adipocyte differentiation and obesity-induced inflammation. SlimTrym® inhibited mitotic clonal expansion (MCE) of 3T3-L1 adipocytes by inducing G1 cell cycle arrest via upregulation of p21 and p53. SlimTrym® attenuated adipogenic differentiation by downregulating adipogenic factors, such as CCAAT-enhancer-binding proteins (C/EBPs) and peroxisome proliferator-activated receptor γ (PPARγ), and upregulating AMP-activated protein kinase (AMPK). Pretreatment with compound C significantly reduced SlimTrym®-mediated suppression of lipid accumulation. SlimTrym® reduced the expression of pro-inflammatory cytokines, including monocyte chemoattractant protein 1 (MCP-1), interleukin (IL)-1ß and IL-6, in co-cultured 3T3-L1 adipocytes and RAW264.7 macrophages. C57BL/6 mice administered with SlimTrym® for 16 weeks showed markedly reduced high-fat diet (HFD)-induced infiltration of monocytes/macrophages in adipose tissue; however, the level of M2 macrophage markers (CD163 and IL-10) was increased. Taken together, these findings indicate that SlimTrym® exerts both anti-adipogenic and anti-inflammatory effects, and can potentially treat obesity and adipose tissue inflammation.

Pseudogene RACGAP1P activates RACGAP1/Rho/ERK signalling axis as a competing endogenous RNA to promote hepatocellular carcinoma early recurrence.

Accumulating evidence has indicated crucial roles for pseudogenes in human cancers. However, the roles played by pseudogenes in the pathogenesis of HCC, particularly HCC early recurrence, still incompletely elucidated. Herein, we identify a novel early recurrence related pseudogene RACGAP1P which was significantly upregulated in HCC and was associated with larger tumour size, advanced clinical stage, abnormal AFP level and shorter survival time. In vitro and in vivo experiments have shown that RACGAP1P is a prerequisite for the development of malignant characteristics of HCC cells, including cell growth and migration. Mechanistic investigations indicated that RACGAP1P elicits its oncogenic activity as a ceRNA to sequestrate miR-15-5p from its endogenous target RACGAP1, thereby leading to the upregulation of RACGAP1 and the activation of RhoA/ERK signalling. These results may provide new insights into the functional crosstalk of the pseudogene/miRNA/parent-gene genetic network during HCC early relapse and may contribute to improving the clinical intervention for this subset of HCC patients.

[Clinical analysis of 51 cases of atypical measles syndrome characterized by fever and multiple lung lesions].

OBJECTIVE: To investigate the clinical and chest radiological features of atypical measles syndrome (AMS), and therefore to improve the recognition and diagnosis of the disease. METHODS: The clinical features, laboratory tests and chest radiological manifestations of 51 cases of outbreak AMS in one high school of Shanxi province were retrospectively analyzed. RESULTS: There were 31 males and 20 females, aging 18 - 33 years old. The main clinical presentations included fever (50/51), headache and dizziness (44/51), fatigue (31/51), nasal discharge (1/51), sore throat (10/51), cough (5/51), dyspnea (3/51), dacryorrhea (13/51), Koplik's spots (1/51), and skin rash (18/51) which were mostly congested maculopapules and firstly appeared on the hands, the feet and the back. Laboratory tests showed that the peripheral WBC count was in the normal range in most of the patients (n = 39), and lower than normal in 7 cases. The percentage of lymphocytes was less than 20% in 29, 20% - 40% in 20, and higher than 40% in 2 cases. The percentage of neutrophils was higher than 70% in 33 cases. Abnormal urinalysis (13/51) included positive urine protein and OB. High CRP (36/51), abnormal liver function (2/51), and abnormal renal function (1/51) were also observed. Forty-eight cases showed abnormal chest CT, manifested mostly as bilateral multiple lesions of different sizes and low density nodules and patchy areas, distributed randomly from apex to base, and from the middle zone to the pleura. CONCLUSIONS: The clinical manifestation of AMS is atypical, characterized by the lower incidence of catarrh symptom and skin rashes with atypical appearance, but higher incidence of lung lesions. Familiarity with the atypical clinical manifestations and radiological features of AMS, epidemiological study and measles antibody detection are important for rapid and accurate diagnosis of the disease.

p68 prompts the epithelial-mesenchymal transition in cervical cancer cells by transcriptionally activating the TGF-ß1 signaling pathway.

Overexpression of p68 has been reported in various types of cancer. However, little study has been conducted on the expression and role of p68 in cervical cancer. Therefore, the present study focuses on the role of p68 in cervical cancer cells, which may elucidate its potential mechanism of cervical cancer progression and shed light on the precision medical treatment of cervical cancer. Firstly, the expression of p68 was analyzed using reverse transcription-quantitative polymerase chain reaction and western blot analysis. The changes to cell morphology were observed using an inverted microscope (XDS-500D; Shanghai Caikon Optical Instrument Co., Ltd., Shanghai, China). Cell migration was determined using an in vitro scratch assay. The present study demonstrated that the mRNA and protein levels of p68 were significantly enhanced in cervical cancer CaSki, HeLa [human papillomavirus (HPV)-18-positive], SiHa (HPV-16-positive) and C-33A (HPV-negative) cell lines compared with the human keratinocyte HaCaT cell line. Overexpression of p68 induced an elongated and spindle-shaped morphology in CaSki cells. Upregulation of p68 increased the expression of α-smooth muscle actin, vimentin and fibronectin however, epithelial marker E-cadherin was significantly decreased. Furthermore, the in vitro scratch assay demonstrated that overexpression of p68 markedly enhanced CaSki cell migration capacity at 24 and 48 h. Knockdown of p68 partially reversed transforming growth factor-ß1 (TGF-ß1)-induced changes in epithelial-mesenchymal transition (EMT) markers and cell morphological changes. In summary, the present study demonstrated that p68 transcriptionally activated the expression of TGF-ß1, thereby prompting EMT in cervical cancer cells.