Long-Term Effects of Extended Upper Blepharoplasty Combined With Subbrow Skin Removal for Correction of Lateral Hooding in Asian Women.

Upper eyelid aging with lateral hooding is common among Asian women older than 40 years. Since Asians tend to develop more visible scars than White people, we used an extended upper blepharoplasty technique to correct lateral hooding and conceal the scar, combined with the removal of the thick subbrow skin for women over 60 years of age, to achieve a stable, improved outcome. An extended cutaneous scalpel-shaped excision was designed and hid the extended part of the excision in the patient's upward crow's feet to address the redundant skin of lateral hooding. For patients older than 60 years, we used a crescent-shaped excision and simultaneously removed the thick skin under the eyebrow to reduce the likelihood of long-term postoperative pseudoexcess. A retrospective study was conducted on 40 Asian women who underwent upper eyelid rejuvenation surgery with the above methods from July 2020 to March 2021 (follow-up, 12-15 mo). Extended blepharoplasty notably corrected the lateral hooding and achieved a natural double eyelid. The postoperative scar was inconspicuous. For patients older than 60 years, the long-term rejuvenation outcome was stable when associated with subbrow skin removal. However, two patients older than 60 years in whom the subbrow skin was not removed developed pseudoexcess of the upper eyelid 1 year postoperatively. Extended blepharoplasty is a simple and effective technique for improving periorbital aging in Asian women, and the postoperative scarring was inconspicuous. For patients older than 60 years, we recommend removal of the thick subbrow skin to avoid long-term postoperative pseudoexcess.

Blocking stanniocalcin 2 reduces sunitinib resistance in clear cell renal cell carcinoma.

Stanniocalcin 2 (STC2) has been identified as a prognostic marker in renal cell carcinoma. However, the role of STC2 in renal cell carcinoma is still unclear. In this study, we investigated the relationship between high expression of STC2 and sunitinib resistance in cells and the underlying mechanism. Through GEPIA platform analysis based on TCGA database, it showed that the expression of STC2 in kidney renal clear cell carcinoma (KIRC) was significantly higher than that in the normal population. Real-time quantitative PCR and western blotting detected significantly higher expression levels of STC2 in clear cell renal cell carcinoma (ccRCC) cells than that in normal renal cells. Enzyme-linked immunosorbent assay (ELISA) determined whether there is a high secretion of STC2 in ccRCC cells. The sunitinib resistance could be significantly reduced by STC2 neutralizing antibody but aggravated by the addition of recombinant human STC2 in ccRCC cells. Sunitinib suppressed STC2 expression and secretion, destroyed lysosomal acidic pH, and accumulated in the cells. However, STC2 neutralizing antibody can reduce the accumulation of sunitinib in cells to improve the inhibitory efficiency of sunitinib on cell proliferation. This study suggested STC2 could serve as a potential novel target for the treatment of ccRCC, anti-STC2 antibody might be an option of immunotherapy in the future.

Whole-Exon Sequencing and Correlation Analysis of a 14-Month-Old Girl With Orofaciodigital Syndrome.

Orofaciodigital syndrome type 1 (OFDS1) is a genetic disorder characterized by specific oral, facial, and limb malformations. A 14-month-old girl with congenital cleft palate, lower lip midline cleft, and digital anomalies admitted to our hospital was preliminarily diagnosed with OFDS1. Genetic analysis revealed that she carried a heterozygous variant of OFD1 at locus Xp22.2 on the X chromosome. Herein, we present the specific phenotype and genotype and the treatment modalities for this patient and references for diagnosing and treating OFDS.

Low microRNA-139 expression associates with poor prognosis in patients with tumors: A meta-analysis.

BACKGROUND: microRNA-139 (miR-139) is dysregulated in various types of tumors and plays a key role in carcinogenesis. miR-139 may be used as a diagnostic and prognostic biomarker of cancers. However, the data from the literature are not consistent. The present study aimed to verify the prognostic and diagnostic values of miR-139 in solid tumors. DATA SOURCES: PubMed, Web of Science and Embase databases were searched and publications from January 2011 to August 2017 were included. We used Gene Expression Omnibus (GEO) and The Cancer Genome Atlas (TCGA) database to further validate this meta-analysis. RESULTS: Eight individual studies from seven articles were included. Pooled analyses showed that low miR-139 expression was related to worse overall survival (OS) [hazard ratio (HR) = 2.27; 95% confidence intervals (CI): 1.74-2.95; P < 0.001] in solid tumors, including hepatocellular carcinoma (HCC) and glioblastoma multiforme (GBM), consisting with the results of TCGA. However, our results of CRC showed that low miR-139 expression was associated with poor OS which was contradictory with the results in TCGA database and need larger samples to validate the phenomenon; whereas for CRC patients, high miR-139 expression predicted poor RFS, which was in good accordance with TCGA results. The results of 27 microarrays from GEO database showed that miR-139 expression levels were lower in tumor tissues compared to adjacent non-tumor tissues or healthy tissues. Decreased miR-139 expression was also significantly correlated with poor differentiation grade (OR = 3.57; 95% CI: 1.44-8.85; P = 0.006). However, the combined data indicated that no associations between miR-139 expression and the following parameters such as age (pooled OR = 1.50; 95% CI: 0.69-3.24; P = 0.304), gender (pooled OR = 0.92; 95% CI: 0.56-1.51; P = 0.738), tumor size (pooled OR = 1.51; 95% CI: 0.69-3.31; P = 0.298), late tumor-node-metastasis stage (pooled OR = 1.63; 95% CI: 0.99-2.68; P = 0.057) and lymph-node-metastasis (pooled OR = 0.66; 95% CI: 0.34-1.28; P = 0.222). CONCLUSIONS: Low miR-139 expression was related to poor prognosis in HCC and GBM, which could be regarded as a potential prognostic biomarker. However, its precise functional role in CRC still need to be further investigated through larger samples and multicenter studies.

Rapamycin enhances the anti-angiogenesis and anti-proliferation ability of YM155 in oral squamous cell carcinoma.

YM155, a small molecule inhibitor of survivin, has been studied in many tumors. It has been shown that YM155 inhibited oral squamous cell carcinoma through promoting apoptosis and autophagy and inhibiting proliferation. It was found that YM155 also inhibited the oral squamous cell carcinoma-mediated angiogenesis through the inactivation of the mammalian target of rapamycin pathway. Rapamycin, a mammalian target of rapamycin inhibitor, played an important role in the proliferation and angiogenesis of oral squamous cell carcinoma cell lines. In our study, cell proliferation assay, transwell assay, tube formation assay, and western blot assay were used to investigate the synergistic effect of rapamycin on YM155 in oral squamous cell carcinoma. Either in vitro or in vivo, rapamycin and YM155 exerted a synergistic effect on the inhibition of survivin and vascular endothelial growth factor through mammalian target of rapamycin pathway. Overall, our results revealed that low-dose rapamycin strongly promoted the sensitivity of oral squamous cell carcinoma cell lines to YM155.

Curcumin Reduces Tumour Necrosis Factor-Enhanced Annexin V-Positive Microparticle Release in Human Vascular Endothelial Cells.

PURPOSE: Circulating microparticles have been highlighted as biomarkers of cardiovascular disease state and progression. The aim of this study was to evaluate the effects of curcumin on microparticle release from endothelial cells undergoing TNF-induced cell activation and apoptosis. METHODS: This study evaluated the effects of curcumin on microparticle release, cytotoxicity, apoptosis, cell adhesion molecule expression and monocyte adhesion in EAhy926 human endothelial cells. RESULTS: The results showed that the numbers of microparticles were increased by tumour necrosis factor (TNF) or the combination of TNF and cycloheximide (CHX). Curcumin attenuated microparticle release caused by TNF or TNF plus CHX treatments. The pretreatment by curcumin not only negated the accelerated cell death and apoptosis caused by TNF and CHX, but also diminished TNF-induced cell activation, as assessed by reduced surface expression of intercellular adhesion molecule 1, and adhesion of monocytes to endothelial monolayers. CONCLUSION: Curcumin reduced microparticle release from endothelial cells undergoing cell activation and apoptosis, which supports its protective role in TNF-associated endothelial dysfunction, and highlights its potential use as a nutraceutical agent for vascular inflammatory diseases. This article is open to POST-PUBLICATION REVIEW. Registered readers (see "For Readers") may comment by clicking on ABSTRACT on the issue's contents page.

Seasonal Variation of Triterpenes and Phenolic Compounds in Australian Centella asiatica (L.) Urb.

INTRODUCTION: Specific triterpenes, phenolic acids and flavonoids in Centella asiatica have been found to be bioactive. Harvesting the plant when these putative bioactive compounds are at their highest concentrations would provide consistency in their chemical profile, thus ensuring the quality and efficacy of derived medicinal products. OBJECTIVE: The aim of the study was to determine the impact of harvesting time on the contents of major triterpenoid and phenolic compounds in C. asiatica. METHODOLOGY: Australian C. asiatica was collected from a designated area in different months. The principal triterpenes (asiaticoside, madecassoside, asiatic acid and madecassic acid), flavonoid compounds (rutin, quercetin and kaempferol) and chlorogenic acid were quantitatively determined by HPLC-DAD analysis. RESULTS: Triterpenoid, kaempferol and chlorogenic acid content showed significant variation (p < 0.05) in different collecting months. The total content of the four triterpenes reached its highest levels in January and February (83.15 ± 0.16 mg/g and 78.41 ± 0.16 mg/g, respectively), the summer season of the southern hemisphere, and their lowest values in winter (June) and spring (October) seasons (35.65 ± 0.20 and 35.50 ± 0.55 mg/g, respectively). Similarly, the contents of chlorogenic acid and kaempferol were the highest in December and January (1.62 ± 0.01 and 0.33 ± 0.01 mg/g, respectively), and the lowest in June (0.06 ± 0.01 and 0.09 ± 0.01 mg/g, respectively). CONCLUSION: The results indicate that harvesting C. asiatica in summer returns the highest yield of the target triterpenoids, kaempferol and chlorogenic acid.

The effectiveness of a structured educational intervention on disease-related misconception and quality of life in patients with irritable bowel syndrome.

A significant number of patients with irritable bowel syndrome hold misconceptions about their disease and experience more impaired quality of life compared with the general population and people suffering from other chronic diseases. This study was designed to explore the effectiveness of a structured educational intervention on disease-related misconceptions and quality of life in patients with irritable bowel syndrome in Wuhan, China. A convenience sample of 23 patients with irritable bowel syndrome participated in an educational program that consisted of 4 weekly sessions in a group setting. Instruments, including an irritable bowel syndrome-related misconception scale and irritable bowel syndrome quality-of-life scale, were used for evaluation at baseline and 3 months after the sessions. Three months after the structured educational intervention, the score for irritable bowel syndrome-related misconception was significantly decreased (p < .001), and the score for irritable bowel syndrome quality of life was significantly improved (p < .001). We conclude that the structured educational intervention seems to be a proper method to reduce the disease-related misconceptions and improve the quality of life in patients with irritable bowel syndrome. Planning and implementing such clinical education programs will be helpful in decreasing disease-related misconceptions and promoting quality of life in patients with irritable bowel syndrome.

A comparative study on the inhibitory effects of different parts and chemical constituents of pomegranate on α-amylase and α-glucosidase.

Pomegranate has been documented for the management of diabetes in Unani and Chinese medicine. This study compared the effects of the extracts of different pomegranate parts, including juice, peels, seeds and flowers, on carbohydrate digestive enzymes (α-amylase and α-glucosidase) in vitro. The methanolic flower extract inhibited α-amylase and α-glucosidase, while the methanolic peel extract inhibited α-glucosidase selectively. The most active flower extract was subjected to water-ethyl acetate partition. The ethyl acetate fraction was more potent than the water fraction in inhibiting both enzymes. Gallic acid and ellagic acid also showed selective inhibition against α-glucosidase, and their presence in the ethyl acetate fraction was confirmed by HPLC-DAD and HPLC-HESI-MS. Our findings suggest that the inhibition of carbohydrate digestive enzymes and their phenolic content may contribute to the anti-hyperglycaemic effects of pomegranate flower and peel, and support their claims in diabetes.

Combination of TNF-α, homocysteine and adenosine exacerbated cytotoxicity in human cardiovascular and cerebrovascular endothelial cells.

Disruption to the vascular homoeostasis is detrimental in vascular diseases. This study examined how the combination of homocysteine, adenosine and tumor necrosis factor-alpha (TNF-α) influenced endothelial cell survival. In cultured human-derived cardiovascular (EA.hy926) and cerebrovascular (HBEC-5i) endothelial cells, cell death events were initiated by TNF-α (0.1-10 ng/mL) only when both homocysteine (0.5 mM) and adenosine (0.5 mM) were present. The accelerated cell death events induced by the combination were triggered through excessive apoptosis. This was evident by membrane phospholipid phosphatidylserine externalisation, cell shrinkage and DNA fragmentation, as well as an increase in the expressions and occurrence of active caspase-3 and cleaved poly(ADP-ribose) polymerase (PARP) positive cells. Collectively, homocysteine, adenosine and TNF-α are interrelated in the survival of endothelial cells, and this co-existence should be considered in future drug development for cardiovascular and cerebrovascular diseases.

Herbal medicines for the management of diabetes.

Herbal medicines have been used in the management of diabetes in traditional medicine. This chapter reviews recent findings of the most popular herbs reported to treat diabetes through their relevant mechanistic pathways. These include increased insulin secretion, improvement in insulin sensitivity, enhanced glucose uptake by adipose and muscle tissues, inhibition of glucose absorption from intestine, inhibition of glucose production from hepatocytes and anti-inflammatory activities. The pharmacological activities have highlighted the potential efficacy of these herbal medicines in the management of diabetes.

Differential behavioural and neurochemical outcomes from chronic paroxetine treatment in adolescent and adult rats: a model of adverse antidepressant effects in human adolescents?

Selective serotonin reuptake inhibitor use is associated with increased risk of suicidal ideation in adolescent humans, yet the neuropharmacological basis of this phenomenon is unknown. Consequently, we examined the behavioural and neurochemical effects of chronic paroxetine (PRX) treatment in adult and adolescent rats. Rats received PRX in their drinking water (target dose 10 mg/kg) for 22 d, during which time they were assessed for depression- and anxiety-like behaviours. Subsequent ex-vivo analyses examined serum PRX concentrations, striatal neurotransmitter content, and regional serotonin and dopamine transporter (SERT, DAT) binding density. After 11-12 d treatment, PRX-treated adolescent rats showed a significant inhibition of social interaction while adults were unaffected. After 19-20 d treatment, adolescents failed to show an antidepressant-like effect of PRX treatment on the forced swim test (FST), while PRX-treated adults showed a typical decrease in immobility and increase in swimming. Two PRX-treated adolescents died unexpectedly after the FST suggesting a compromised response to physical stress. Despite their greater apparent adverse reaction to the drug, adolescents had significantly lower plasma PRX than adults at day 22 of treatment. Chronic PRX treatment had similar effects in adults and adolescents on striatal 5-HT (unchanged relative to controls) and 5-HIAA levels (decreased), while markers of dopaminergic function (DOPAC, HVA, DA turnover) were increased in adults only. SERT density was up-regulated in the amygdala in PRX-treated adolescents only while DAT density in the nucleus accumbens was down-regulated only in PRX-treated adults. These data suggest that the immature rat brain responds differently to PRX and that this might be of use in modelling the atypical response of human adolescents to antidepressants. The age-specific PRX-induced changes in dopaminergic markers and SERT and DAT binding provide clues as to the neural mechanisms underlying adverse PRX effects in adolescent humans.

Parkinsonism and impaired axonal transport in a mouse model of frontotemporal dementia.

Frontotemporal dementia (FTD) is characterized by cognitive and behavioral changes and, in a significant subset of patients, Parkinsonism. Histopathologically, FTD frequently presents with tau-containing lesions, which in familial cases result from mutations in the MAPT gene encoding tau. Here we present a novel transgenic mouse strain (K3) that expresses human tau carrying the FTD mutation K369I. K3 mice develop a progressive histopathology that is reminiscent of that in human FTD with the K369I mutation. In addition, K3 mice show early-onset memory impairment and amyotrophy in the absence of overt neurodegeneration. Different from our previously generated tau transgenic strains, the K3 mice express the transgene in the substantia nigra (SN) and show an early-onset motor phenotype that reproduces Parkinsonism with tremor, bradykinesia, abnormal gait, and postural instability. Interestingly, motor performance of young, but not old, K3 mice improves upon L-dopa treatment, which bears similarities to Parkinsonism in FTD. The early-onset symptoms in the K3 mice are mechanistically related to selectively impaired anterograde axonal transport of distinct cargos, which precedes the loss of dopaminergic SN neurons that occurs in aged mice. The impaired axonal transport in SN neurons affects, among others, vesicles containing the dopamine-synthesizing enzyme tyrosine hydroxylase. Distinct modes of transport are also impaired in sciatic nerves, which may explain amyotrophy. Together, the K3 mice are a unique model of FTD-associated Parkinsonism, with pathomechanistic implications for the human pathologic process.

Attenuation of methylglyoxal-induced glycation and cellular dysfunction in wound healing by Centella cordifolia.

Current pre-clinical evidences of Centella focus on its pharmacological effects on normal wound healing but there are limited studies on the bioactivity of Centella in cellular dysfunction associated with diabetic wounds. Hence we planned to examine the potential of Centella cordifolia in inhibiting methylglyoxal (MGO)-induced extracellular matrix (ECM) glycation and promoting the related cellular functions. A Cell-ECM adhesion assay examined the ECM glycation induced by MGO. Different cell types that contribute to the healing process (fibroblasts, keratinocytes and endothelial cells) were evaluated for their ability to adhere to the glycated ECM. Methanolic extract of Centella species was prepared and partitioned to yield different solvent fractions which were further analysed by high performance liquid chromatography equipped with photodiode array detector (HPLC-PDA) method. Based on the antioxidant [2,2-diphenyl-1-picrylhydrazyl (DPPH) assay] screening, anti-glycation activity and total phenolic content (TPC) of the different Centella species and fractions, the ethyl acetate fraction of C. cordifolia was selected for further investigating its ability to inhibit MGO-induced ECM glycation and promote cellular distribution and adhesion. Out of the three Centella species (C. asiatica, C. cordifolia and C. erecta), the methanolic extract of C. cordifolia showed maximum inhibition of Advanced glycation end products (AGE) fluorescence (20.20 ± 4.69 %, 25.00 ± 3.58 % and 16.18 ± 1.40 %, respectively). Its ethyl acetate fraction was enriched with phenolic compounds (3.91 ± 0.12 mg CAE/µg fraction) and showed strong antioxidant (59.95 ± 7.18 µM TE/µg fraction) and antiglycation activities. Improvement of cells spreading and adhesion of endothelial cells, fibroblasts and keratinocytes was observed for ethyl acetate treated MGO-glycated extracellular matrix. Significant reduction in attachment capacity of EA.hy926 cells seeded on MGO-glycated fibronectin (41.2%) and attachment reduction of NIH3t3 and HaCaT cells seeded on MGO-glycated collagen (33.7% and 24.1%, respectively) were observed. Our findings demonstrate that ethyl acetate fraction of C. cordifolia was effective in attenuating MGO-induced glycation and cellular dysfunction in the in-vitro wound healing models suggesting that C. cordifolia could be a potential candidate for diabetic wound healing. It could be subjected for further isolation of new phytoconstituents having potential diabetic wound healing properties.

Corrigendum: Previous Radiotherapy Increases the Efficacy of IL-2 in Malignant Pleural Effusion: Potential Evidence of a Radio-Memory Effect?

[This corrects the article DOI: 10.3389/fimmu.2018.02916.].

[Immortalized mouse brain endothelial cell line Bend.3 displays the comparative barrier characteristics as the primary brain microvascular endothelial cells].

OBJECTIVE: The purpose of this study was to assess weather the immortalized mouse brain endothelial cell line Bend.3 displays the comparative barrier characteristics as the primary brain microvascular endothelial cells (BEMC). METHODS: Immortalized mouse brain endothelial cell line, Bend.3 cells were cultured in transwell inserts and their restrictive characteristics were assessed by transendothelial electrical resistance (TEER) and horseradish peroxidase (HRP) permeability assays. Western blot and direct fluorescent staining methods were used to detect the tight junction protein expression and F-actin distribution. RESULTS: The TEER in Bend.3 cells increased with the prolonged culture time and increased to 82.3+/-6.0 Omega cm2 10 days after culture, which was significantly higher than that 3 days after culture (37.3+/-3.1 Omega cm2; P<0.05). There were significant differences in the permeability rates for HRP 3 and 10 days after culture (4.3+/-0.20)% vs (2.2+/-0.05)% (P<0.05). Western blot indicated high level expression of tight junction proteins occludin and ZO-1 in Bend.3 cells 10 days after culture. F-actin was visualized around the cell membrane and presented scrobiculate linear fluorescence 10 days after culture. CONCLUSIONS: Bend.3 cells have similar barrier characteristics to BEMC, and their barrier function may reach to the best effect 10 days after culture.

The kainate receptor antagonist UBP310 but not single deletion of GluK1, GluK2, or GluK3 subunits, inhibits MPTP-induced degeneration in the mouse midbrain.

The excitatory neurotransmitter glutamate is essential in basal ganglia motor circuits and has long been thought to contribute to cell death and degeneration in Parkinson's disease (PD). While previous research has shown a significant role of NMDA and AMPA receptors in both excitotoxicity and PD, the third class of ionotropic glutamate receptors, kainate receptors, have been less well studied. Given the expression of kainate receptor subunits GluK1-GluK3 in key PD-related brain regions, it has been suggested that GluK1-GluK3 may contribute to excitotoxic cell loss. Therefore the neuroprotective potential of the kainate receptor antagonist UBP310 in animal models of PD was investigated in this study. Stereological quantification revealed administration of UBP310 significantly increased survival of dopaminergic and total neuron populations in the substantia nigra pars compacta in the acute MPTP mouse model of PD. In contrast, UBP310 was unable to rescue MPTP-induced loss of dopamine levels or dopamine transporter expression in the striatum. Furthermore, deletion of GluK1, GluK2 or GluK3 had no effect on MPTP or UBP310-mediated effects across all measures. Interestingly, UBP310 did not attenuate cell loss in the midbrain induced by intrastriatal 6-OHDA toxicity. These results indicate UBP310 provides neuroprotection in the midbrain against MPTP neurotoxicity that is not dependent on specific kainate receptor subunits.

An injectable bioactive dressing based on platelet-rich plasma and nanoclay: Sustained release of deferoxamine to accelerate chronic wound healing

Delayed diabetic wound healing has placed an enormous burden on society. The key factors limiting wound healing include unresolved inflammation and impaired angiogenesis. Platelet-rich plasma (PRP) gel, a popular biomaterial in the field of regeneration, has limited applications due to its non-injectable properties and rapid release and degradation of growth factors. Here, we prepared an injectable hydrogel (DPLG) based on PRP and laponite by a simple one-step mixing method. Taking advantages of the non-covalent interactions, DPLG could overcome the limitations of PRP gels, which is injectable to fill irregular injures and could serve as a local drug reservoir to achieve the sustained release of growth factors in PRP and deferoxamine (an angiogenesis promoter). DPLG has an excellent ability in accelerating wound healing by promoting macrophage polarization and angiogenesis in a full-thickness skin defect model in type I diabetic rats and normal rats. Taken together, this study may provide the ingenious and simple bioactive wound dressing with a superior ability to promote wound healing.

Previous Radiotherapy Increases the Efficacy of IL-2 in Malignant Pleural Effusion: Potential Evidence of a Radio-Memory Effect?

Preclinical and clinical studies have shown that prior receipt of radiotherapy enhances antitumor immune responses, a phenomenon we call the "radio-memory effect." However, all of the evidence regarding this effect to date comes from work with PD1/PDL1 inhibitors. Here we explored whether this effect also occurs with other forms of immune therapy, specifically interleukin-2 (IL-2). We retrospectively assessed outcomes in patients with malignant pleural effusion (MPE) who had previously received radiotherapy for non-small-cell lung cancer (NSCLC) within 18 months before the intrapleural infusion of IL-2 or cisplatin. Radiotherapy sites included lungs, thoracic lymph nodes, and intracranial. All patients received intrapleural infusion of IL-2 or cisplatin, and most had had several cycles of standard chemotherapy for NSCLC. We identified 3,747 patients with MPE (median age 64 years [range 29-88)) treated at one of several institutions from August 2009 through February 2015; 642 patients had been treated with IL-2 and 1102 with cisplatin and had survived for at least 6 months afterward. Among those who received IL-2, 288 had no radiotherapy, 324 had extracranial (i.e., thoracic) radiotherapy, and 36 had intracranial radiotherapy. The median follow-up time for surviving patients was 38 months. Patients who had received extracranial radiotherapy followed by IL-2 had significantly longer PFS than patients who had not received extracranial radiotherapy (i.e., either no radiotherapy or intracranial radiotherapy). Patients who had received intracranial or extracranial radiotherapy followed by IL-2 had significantly longer OS than did other patients. No survival advantage was noted for prior radiotherapy among patients who received intrapleural cisplatin. We speculate that previous radiotherapy could enhance the efficacy of subsequent intrapleural infusion of IL-2, a "radio-memory" effect that could be beneficial in future studies.

[Epidemiological analysis of malaria in Shandong Province in 2017].

OBJECTIVE: To understand the malaria epidemiological characteristics of Shandong Province in 2017, so as to provide the evidences for formulating targeted prevention and control strategy and measures. METHODS: The data of malaria cases of Shandong Province in 2017 were collected from the Information Management System for Infectious Diseases Report and Information Management System for Parasitic Diseases Control and Prevention. The epidemiological characteristics of malaria situation and the diagnosis and treatment of malaria cases were analyzed. RESULTS: There were 209 malaria cases reported in 2017, all of them were imported cases, and 205 cases (98.09%) were imported from African countries. Among them, 155 cases (74.16%) were falciparum malaria cases. Totally 16 cities had cases reported in 2017, and 154 cases (73.68%) were reported in 6 cities (Yantai, Jining, Weihai, Dezhou, Qingdao, and Tai'an). The malaria cases distributed in 17 cities, and there were 110 cases distributed in 4 cities, namely Yantai, Tai'an, Weihai, and Qingdao, which accounted for 56.41% of the total cases in Shandong Province. Both the median time from onset to seeing a doctor and the median time from seeing a doctor to being diagnosed were one day. Totally 12.92% of the cases went to visit a doctor 7 days later after they had symptoms and 10.53% of the cases were diagnosed 7 days later after the first visit to a doctor. CONCLUSIONS: At present, the prevention and control of the imported malaria is the focus of malaria control in Shandong Province. According to the central tendency of the malaria situation, the health education and propaganda among the high risk groups and the training on the diagnosis and treatment among medical workers should be strengthened, so as to prevent the risk of reappearance of local cases in the past malaria endemic regions, and to ensure the goal of malaria elimination been achieved on schedule.