Effect of turbulence-induced sediment resuspension and sedimentation on underwater wireless optical communication.

In real-life marine environments, the composition and grain size of suspended sediments and the resuspension and sedimentation of sediments caused by turbulence may have a significant impact on underwater wireless optical communication (UWOC). However, to date, researchers have not conducted quantitative research on this issue. To this end, we innovatively study the effects of different compositions and grain sizes of suspended sediments on UWOC and the effects of turbulence-induced sediment resuspension and sedimentation on UWOC in this paper. Quartz and kaolin with different grain sizes are used to simulate sediments in seawater. An oscillating grid that can vary frequency and stroke is used to generate turbulence of different intensities. By comparing the turbidity and optical power density of different simulated sediments with different grain sizes, we find that the smaller the grain size of the simulated sediments, the higher the bit error rate (BER) under the same turbidity. But different simulated sediments with different grain sizes have similar effects on BER performance under the same optical power density. Therefore, turbidity can be used to characterize the changes of underwater channels, and optical power density can be used to evaluate the attenuation of light at the receiving end after transmission through the underwater channel. By continuously changing the frequency of the grid to cause the sediments to resuspend and sink, we prove that the process of turbulence-induced sediment resuspension and sedimentation can seriously affect the BER performance. The larger the frequency of the grid, the greater the turbulence intensity and the worse the BER performance. This study lays a foundation for the practical application of UWOC in mobile ocean observation networks.

Hot-topics cross-propagation and opinion-transfer dynamics in the Chinese Sina-microblog social media: A modeling study.

On social media platforms, hot topics often contain several pieces of related information that can influence internet users, generating either positive or negative opinion orientation. Some of them will choose to retain or change their original opinions after exposure to multiple related messages. To describe the opinion-transfer transient and collective behaviors in this scenario, this paper proposes an opinion-transfer susceptible-forwarding-immunized (OT-SFI) information cross-propagation model. Real multiple information in messages with opinions obtained from the Chinese Sina microblog is used for data fitting to illustrate how model parameters can be estimated and used to predict the accumulative numbers of users with a particular view. The study attempts to relate changes in group views in the network to initial opinion distribution and individuals' opinion choices at the macro level. Furthermore, the model parameters at the micro level are used to measure the probability of "retention" and "reversal" of views in events, as well as the extent to which the masses are influenced by new information views. The result illustrates that the viewpoint distribution of the initial message and the opinion selection of the new message opinion leaders play crucial roles in promoting attention to the topic and driving for a desired collective opinion.

Association between glomerular C4d deposition, proteinuria, and disease severity in children with IgA nephropathy.

BACKGROUND: C4d may be used as a marker to evaluate the condition and prognosis of adults with IgA nephropathy, but there have been few studies of children with IgA nephropathy. METHODS: C4d immunohistochemical staining was performed on samples from children with IgA nephropathy with C1q-negative immunofluorescence. The clinical and pathological treatment and prognostic characteristics of children in the C4d-positive and -negative groups were compared. RESULTS: A total of sixty-five children with IgA nephropathy were included in the study and were followed up for an average of 37 months. C4d was mainly deposited along the capillary loops. The urinary protein-to-creatinine ratio (UPCR) in the C4d-positive group was significantly higher than that in the C4d-negative group (3.97 vs. 0.81, P < 0.001), and the average integrated optical density value of each child was positively correlated with the UPCR (r = 0.441, P < 0.001). There was a significant difference in the proportions of children with mesangial hypercellularity (M1) (68.97% vs. 44.44%, P = 0.048) and segmental glomerulosclerosis (S1) (65.52% vs. 33.33%, P = 0.010) between the C4d-positive group and the C4d-negative group. The proportion of children who received immunosuppressants in the C4d-positive group was higher than that in the C4d-negative group (86.21% vs. 36.11%, P < 0.001). There was no significant difference in the proportion of children developing kidney failure between the two groups. CONCLUSION: C4d was found to be associated with proteinuria, segmental lesions, and immunosuppressant treatment. Activation of the lectin pathway may reflect the severity of clinical and pathological manifestations of IgA nephropathy in children. A higher resolution version of the Graphical abstract is available as Supplementary information.

The application of MDT model for calciphylaxis management in patients with end-stage renal disease.

This study focuses on the application of nurse-led multidisciplinary collaborative therapy (MDT) management model for calciphylaxis prevention of patients with terminal renal disease. Through the establishment of a multidisciplinary management team spanning nephrology department, blood purification center, dermatology department, burn and plastic surgery department, infection department, stem cell platform, nutrition department, pain department, cardiology department, hydrotherapy group, dermatology group, and outpatient treatment room, the distribution of duties among team members were clarified to bring out the best advantages of a multidisciplinary teamwork during treatment and nursing. For patients with calciphylaxis symptoms in terminal renal disease, a case-by-case management model was carried out with the focus on personalised problem. We emphasised on personalised wound care, precise medication care, active pain management, psychological intervention and palliative care, the amelioration of calcium and phosphorus metabolism disorder, nutritional supplementation, and the therapeutic intervention based on human amniotic mesenchymal stem cell regeneration. The MDT model effectively compensates for traditional nursing mode and could serve as a novel clinical management modality for calciphylaxis prevention in patients with terminal renal disease.

Suppression of ovarian cancer by low-intensity ultrasound through depletion of IL-6/STAT3 inflammatory pathway-maintained cancer stemness.

Ovarian carcinoma is the key cause of cancer death from gynecological malignancy of women. Chemotherapy-resistance, metastasis and relapse contribute to the high mortality in ovarian cancer patients. Cancer stem cells (CSCs) stand for the root of kinds of cancer types such as ovarian cancer, are the key driver of tumor initiation, cancer metastasis, and resistance to conventional chemotherapy as well as genomic targeted therapy. Thus, the approach to eliminate CSCs and uncovering the mechanism will have substantial impact on cancer therapy. However, targeting CSC remains unfeasible in clinical practice in ovarian cancer therapy. In this study, we first found that Low-intensity ultrasound (LIUS) was capable of reducing the CSC populations in the xenograft model with ovarian cancer, with blocking survival, anti-apoptosis, self-renewal, and downregulating the cancer stemness genes in ovarian CSCs. Moreover, LIUS ameliorated IL-6/STAT3 inflammatory pathway via inhibiting IL-6-induced STAT3 phosphorylation, DNA binding activity and, the expressions of its downstream effectors in ovarian CSCs while no explicit effect was found in the corresponding bulk cancer cells. Additional approaches in molecular studies showed that LIUS disrupts CSC features via inhibiting IL-6/STAT3 inflammatory pathway. Collectively, our data for the first time elucidate IL-6/STAT3 inflammatory loop as the key CSC or cancer stemness pathway in ovarian cancer by LIUS treatment, providing a novel and potential therapy and a promising target in ovarian cancer.

mTOR and Beclin1: Two key autophagy-related molecules and their roles in myocardial ischemia/reperfusion injury.

Autophagy is the general term of lysosomal degradation of substances in cells, which is considered the key to maintaining the normal structure and function of the heart. It also has a correlation with several heart diseases, in particular, myocardial ischemia/reperfusion (I/R) injury. At the stage of myocardial ischemia, autophagy degrades nonfunctional cytoplasmic proteins providing the critical nutrients for the critical life activities, thereby suppressing cell apoptosis and necrosis. However, autophagy is likely to affect the heart negatively in the reperfusion stage. Mammalian target of rapamycin (mTOR) and Beclin1 are two vital autophagy-related molecules in myocardial I/R injury playing significant roles in different stages. In the ischemia stage, mTOR plays its roles through AMPK/mTOR and phosphoinositide 3-kinase/Akt/mTOR pathway, whereas Beclin1 plays its roles through its upregulation in the reperfusion stage. A possible interaction between mTOR and Beclin1 has been reported recently, and further studies need to be done to find the underlying interaction between the two molecules in myocardial I/R injury.

Oroxin B selectively induces tumor-suppressive ER stress and concurrently inhibits tumor-adaptive ER stress in B-lymphoma cells for effective anti-lymphoma therapy.

Cancer cells have both tumor-adaptive and -suppressive endoplasmic reticulum (ER) stress machineries that determine cell fate. In malignant tumors including lymphoma, constant activation of tumor-adaptive ER stress and concurrent reduction of tumor-suppressive ER stress favors cancer cell proliferation and tumor growth. Current ER stress-based anti-tumor drugs typically activate both tumor-adaptive and -suppressive ER stresses, resulting in low anti-cancer efficacy; hence, selective induction of tumor-suppressive ER stress and inhibition of tumor-adaptive ER stress are new strategies for novel anti-cancer drug discovery. Thus far, specific tumor-suppressive ER stress therapeutics have remained absent in clinical settings. In this study, we explored unique tumor-suppressive ER stress agents from the traditional Chinese medicinal herb Oroxylum indicum, and found that a small molecule oroxin B selectively induced tumor-suppressive ER stress in malignant lymphoma cells, but not in normal cells, effectively inhibited lymphoma growth in vivo, and significantly prolonged overall survival of lymphoma-xenografted mice without obvious toxicity. Mechanistic studies have revealed that the expression of key tumor-adaptive ER-stress gene GRP78 was notably suppressed by oroxin B via down-regulation of up-stream key signaling protein ATF6, while tumor-suppressive ER stress master gene DDIT3 was strikingly activated through activating the MKK3-p38 signaling pathway, correcting the imbalance between tumor-suppressive DDIT3 and tumor-adaptive GRP78 in lymphoma. Together, selective induction of unique tumor-suppressive ER stress and concurrent inhibition of tumor-adaptive ER stress in malignant lymphoma are new and feasible approaches for novel anti-lymphoma drug discovery and anti-lymphoma therapy.

Dehydroeffusol effectively inhibits human gastric cancer cell-mediated vasculogenic mimicry with low toxicity.

Accumulated data has shown that various vasculogenic tumor cells, including gastric cancer cells, are able to directly form tumor blood vessels via vasculogenic mimicry, supplying oxygen and nutrients to tumors, and facilitating progression and metastasis of malignant tumors. Therefore, tumor vasculogenic mimicry is a rational target for developing novel anticancer therapeutics. However, effective antitumor vasculogenic mimicry-targeting drugs are not clinically available. In this study, we purified 2,7-dihydroxyl-1-methyl-5-vinyl-phenanthrene, termed dehydroeffusol, from the traditional Chinese medicinal herb Juncus effusus L., and found that dehydroeffusol effectively inhibited gastric cancer cell-mediated vasculogenic mimicry in vitro and in vivo with very low toxicity. Dehydroeffusol significantly suppressed gastric cancer cell adhesion, migration, and invasion. Molecular mechanistic studies revealed that dehydroeffusol markedly inhibited the expression of a vasculogenic mimicry master gene VE-cadherin and reduced adherent protein exposure on the cell surface by inhibiting gene promoter activity. In addition, dehydroeffusol significantly decreased the expression of a key vasculogenic gene matrix metalloproteinase 2 (MMP2) in gastric cancer cells, and diminished MMP2 protease activity. Together, our results showed that dehydroeffusol effectively inhibited gastric cancer cell-mediated vasculogenic mimicry with very low toxicity, suggesting that dehydroeffusol is a potential drug candidate for anti-gastric cancer neovascularization and anti-gastric cancer therapy.

Suberoylanilide hydroxamic acid, an inhibitor of histone deacetylase, suppresses vasculogenic mimicry and proliferation of highly aggressive pancreatic cancer PaTu8988 cells.

BACKGROUND: Pancreatic cancer is one of the most aggressive human malignancies with a extremely low 5-year survival rate. Hence, the search for more effective anti-pancreatic cancer agents is urgent. METHODS: PaTu8988 pancreatic cancer cells were treated with different concentrations of suberoylanilide hydroxamic acid (SAHA), cell survival, proliferation, migration and vasculogenic mimicry (VM) were analyzed. Associated signaling changes were also analyzed by RT-PCR and Western blots. RESULTS: Here, we reported that SAHA, a histone deacetylase inhibitor (HDACi), exerted significant inhibitory efficiency against pancreatic cancer cell survival, proliferation, migration and VM. SAHA dose-dependently inhibited PaTu8988 pancreatic cancer cell growth with the IC-50 of 3.4 ± 0. 7 µM. Meanwhile, SAHA suppressed PaTu8988 cell cycle progression through inducing G2/M arrest, which was associated with cyclin-dependent kinase 1 (CDK-1)/cyclin-B1 degradation and p21/p27 upregulation. Further, SAHA induced both apoptotic and non-apoptotic death of PaTu8988 cells. Significantly, SAHA suppressed PaTu8988 cell in vitro migration and cell-dominant tube formation or VM, which was accompanied by semaphorin-4D (Sema-4D) and integrin-ß5 down-regulation. Our evidences showed that Akt activation might be important for Sema-4D expression in PaTu8988 cells, and SAHA-induced Sema-4D down-regulation might be associated with Akt inhibition. CONCLUSIONS: This study is among the first to report the VM formation in cultured human pancreatic cancer cells. And we provided strong evidence to suggest that SAHA executes significant anti-VM efficiency in the progressive pancreatic cancer cells. Thus, SAHA could be further investigated as a promising anti-pancreatic cancer agent.

TET2 regulation of alcoholic fatty liver via Srebp1 mRNA in paraspeckles.

Epigenetic modifications have emerged as key regulators of metabolism-related complex diseases including the alcoholic fatty liver disease (AFLD) prevalent chronic liver disorder with significant economic implications. Building upon previous research that emphasizes ten-eleven translocation (TET) proteins' involvement in adipocyte insulin sensitization and fatty acid oxidation, we explored the role of TET2 protein in AFLD pathogenesis which catalyzes 5-methylcytosine into 5-hydroxymethylcytosine in DNA/RNA. Our findings revealed that TET2 deficiency exacerbates AFLD progression. And TET2 influenced the expression and activity of sterol regulatory element binding protein 1 (SREBP1), a key regulator of hepatic lipid synthesis, by modulating Srebp1 mRNA retention. Employing RIP-qPCR and bisulfite sequencing techniques, we provided evidence of TET2-mediated epigenetic modifications on Srebp1 mRNA, thereby affecting lipid metabolism. Through elucidating the role of methylation in RNA nuclear retention via paraspeckles, our study enhances understanding of AFLD pathogenesis from an epigenetic perspective, paving the way for identifying potential therapeutic targets.

Jatrorrhizine hydrochloride inhibits the proliferation and neovascularization of C8161 metastatic melanoma cells.

Malignant melanoma is the most aggressive form of skin cancer. Although various antimelanoma approaches have been used in the clinics to treat the disease over the last three decades, none of the drugs significantly prolonged the survival of metastatic melanoma patients; hence, effective drugs against metastatic melanoma are highly desired. In this study, we explored an antimetastatic melanoma agent derived from traditional Chinese medicinal herbs and found that jatrorrhizine hydrochloride (JH), an active component of the traditional Chinese medicinal herb Coptis chinensis, inhibited the proliferation and neovascularization of C8161 human metastatic melanoma cells. JH suppressed C8161 cell proliferation in a dose-dependent manner, with a half-maximal inhibitory concentration of 47.4±1.6 µmol/l; however, it did not induce significant cellular apoptosis at doses up to 320 µmol/l. Mechanistic studies showed that JH-induced C8161 cell cycle arrest at the G0/G1 transition, which was accompanied by overexpression of the cell cycle-suppressive genes p21 and p27 at higher doses. Moreover, JH reduced C8161 cell-mediated neovascularization in vitro and in vivo and impeded the expression of the gene for VE-cadherin, a key protein in tumor vasculogenic mimicry and angiogenesis. Taken together, the effective inhibitory effects of JH on metastatic melanoma cell proliferation and neovascularization with low toxicity suggest that JH is a potential new antimelanoma drug candidate.

The expression of malarial invasion-related molecules is affected by two different nitric oxide-based treatments.

The host immune response to parasitic infections plays an important role in controlling multiplication of the parasite and reducing clinical symptoms and life-threatening complications. Nitric oxide (NO), an important innate immune factor and classic Th1 immune effector, may play a role in inhibiting plasmodium infection. In this study, we used two different approaches (L-Arginine [precursor of NO] and NOC5 [short-time NO donor]) to prove the roles of NO in malaria infection. We used 6-8 week-old female BALB/c mice infected with the rodent malaria Plasmodium yoelii Landau, Michel et Adam, 1968 - strain 17XL (P.y17XL) as a model. For L-Arg treatment, mice were administered with an oral dose of 1.5 mg/g L-Arg daily for seven consecutive days prior to infection with Py17XL. L-Arg pretreatment resulted in the decrease of the mRNA level of the apical membrane antigen 1 (AMA1) gene, which encodes a protein involved in host invasion. For NOC5 treatment, NOC5 was injected intraperitoneally into the P.y17XL infected mice on day 5 post-infection or incubated in vitro with purified Py17XL schizonts. Both in vivo and in vitro treatments with NOC5 led to down-regulation of the transcript and protein levels of invasion-related molecules (AMA1, merozoites surface protein 1 and Py235). Our results confirmed the protective role of NO in the asexual blood stage of parasitic infection, which may be partially due to reduced expression of parasite invasion molecules.

Age-related CD4(+)CD25(+)Foxp3(+) regulatory T-cell responses during Plasmodium berghei ANKA infection in mice susceptible or resistant to cerebral malaria.

Different functions have been attributed to CD4(+)CD25(+)Foxp3(+) regulatory T-cells (Tregs) during malaria infection. Herein, we describe the disparity in Treg response and pro- and anti-inflammatory cytokines during infection with Plasmodium berghei ANKA between young (3-week-old) and middle-aged (8-month-old) C57BL/6 mice. Young mice were susceptible to cerebral malaria (CM), while the middle-aged mice were resistant to CM and succumbed to hyperparasitemia and severe anemia. The levels of pro-inflammatory cytokines, such as TNF-α, in young CM-susceptible mice were markedly higher than in middle-aged CM-resistant mice. An increased absolute number of Tregs 3-5 days post-inoculation, co-occurring with elevated IL-10 levels, was observed in middle-aged CM-resistant mice but not in young CM-susceptible mice. Our findings suggest that Treg proliferation might be associated with the suppression of excessive pro-inflammatory Th1 response during early malaria infection, leading to resistance to CM in the middle-aged mice, possibly in an IL-10-dependent manner.

AhR agonist tapinarof ameliorates lupus autoimmunity by suppressing Tfh cell differentiation via regulation of the JAK2-STAT3 signaling pathway.

BACKGROUND: The aryl hydrocarbon receptor (AhR) is a critical regulator of the pathogenesis of autoimmune disorders. We aimed to investigate the therapeutic effect of the AhR agonist tapinarof during the development of systemic lupus erythematosus (SLE). METHODS: MRL/lpr mice were intraperitoneally injected with 1 or 5 mg/kg tapinarof for 6 weeks. Kidney histopathology was evaluated using hematoxylin and eosin (H&E) and Periodic-Acid-Schiff (PAS) staining. Immunofluorescence microscopy was performed to detect immune complex renal depositions. Flow cytometry (FCM) analysis was carried out to determine the proportions of T and B cell subsets. Realtime qPCR was used to quantify the expression of Tfh cell-associated genes. We conducted an in vitro polarization experiment to observe the effect of tapinarof on Tfh differentiation. Western blotting was used to detect the expression of target proteins. RESULTS: We found that tapinarof treatment ameliorated lupus phenotypes, including splenomegaly, lymph node enlargement, kidney damages, immune complex deposition, and excessive secretion of antibodies. Additionally, we showed that Treg subpopulation frequencies significantly increased in MRL/lpr mice treated with tapinarof, while the proportion of Th1/Th2 cells was reduced after tapinarof administration. Moreover, tapinarof suppressed Tfh cell differentiation and germinal center (GC) reaction in vivo. The inhibitory effect of tapinarof on Tfh cells was further verified in the in vitro Tfh cell polarization experiment. Realtime qPCR revealed that tapinarof repressed the expression of Tfh signature genes. Mechanistically, tapinarof significantly inhibited the phosphorylation levels of JAK2 and STAT3. The capacity for Tfh differentiation was partially rescued by the STAT3 activator Colivelin TFA. Furthermore, our in vitro Tfh polarization experiments indicated that tapinarof suppressed Tfh cell development in SLE. CONCLUSIONS: Our data demonstrated that tapinarof modulated the JAK2-STAT3 pathway to suppress Tfh cell differentiation for the treatment of lupus symptoms in MRL/lpr mice.

Clinical significance and correlation of compliance to thirst in maintenance hemodialysis patients.

BACKGROUND: The main treatment method for end-stage renal disease (ESRD) is maintenance hemodialysis (MHD). With the continuous improvement of dialysis technology, the survival period of MHD patients has been effectively prolonged, but dialysis technology still cannot completely replace renal function. OBJECTIVE: To study the dietary compliance and its correlation with thirst in MHD patients and to provide guidance for clinical development of corresponding intervention countermeasures. METHODS: A total of 90 patients who received MHD treatment from March 2021 to March 2022 were selected as objects. The Renal Adherence Attitudes Questionnaire (RAAQ) and the Renal Adherence Behaviour Questionnaire (RABQ) were used to analyze the dietary compliance and thirst status of patients. Pearson correlation analysis was used to analyze the correlation between diet compliance and thirst. RESULTS: Positive correlations were found between VAS and DTI, SXI and TDS (P< 0.05). Social restrictive attitude was positively correlated with VAS, DTI, SXI, TDS, acceptance attitude and compliance in facing difficulties (P< 0.05), and negatively correlated with self-care compliance (r=-0.35, P< 0.05). Health attitude was positively correlated with VAS, DTI and SXI (P< 0.05). Acceptance attitude was positively correlated with DTI, SXI and TDS (P< 0.05). High RAAQ was associated with high VAS (b= 0.11, 95% CI: 0.05, 0.18), DTI (b= 0.28, 95% CI: 0.17, 0.38), SXI (b= 0.24, 95% CI: 0.14, 0.34) and TDS (b= 0.26, 95% CI: 0.13, 0.4). CONCLUSION: The overall performance of dietary compliance in patients with MHD is at a moderate level, and dietary compliance is negatively correlated with disease perception.

Arcuate Src activation-induced phosphorylation of NR2B NMDA subunit contributes to inflammatory pain in rats.

The tyrosine kinases of Src family play an important role in the central sensitization following peripheral inflammation. However, whether the Src family in the arcuate nucleus (ARC) of mediobasal hypothalamus is involved in central sensitization remains unknown. The aim of this study was to investigate the role and mechanisms of tyrosine kinases of Src family in N-methyl-d-aspartate (NMDA) receptor activity in the ARC following peripheral inflammation. Peripheral inflammation was induced by unilateral injection of complete Freund's adjuvant (CFA) into rat hindpaw. The neuronal activities of the ARC were recorded using electrophysiological field recording from the in vitro mediobasal hypothalamic slices from control and CFA rats. Expression of total and phosphorylated Src and NR2B subunit protein was analyzed by Western blot and immuoprecipitation. Our results showed that CFA injection resulted in an increase in mechanical and thermal sensitivity, which was partially blocked by neonatal monosodium glutamate treatment. CFA injection also enhanced spontaneous firings of ARC neurons, which were reversed by the NMDA receptor NR2B subunit specific antagonist Ro25-6981 and by PP2, an Src family tyrosine kinase inhibitor. In addition, peripheral inflammation enhanced Src phosphorylation and NMDA receptor NR2B subunit phosphorylation without alteration of total NR2B subunit expression in the ARC. Peripheral inflammation also increased the association of NR2B protein with p-Src protein in the ARC. Administration of PP2 blocked the upregulation of NR2B phosphorylation induced by CFA injection. Taken together, our present results suggest that the arcuate Src activation-induced tyrosine phosphorylation of NR2B NMDA subunit may contribute to inflammatory pain.

Polysaccharides from the Chinese medicinal herb Achyranthes bidentata enhance anti-malarial immunity during Plasmodium yoelii 17XL infection in mice.

BACKGROUND: Clinical immunity to malaria in human populations is developed after repeated exposure to malaria. Regulation and balance of host immune responses may lead to optimal immunity against malaria parasite infection. Polysaccharides (ABPS) derived from the Chinese herb ox knee Achyranthes bidentata possess immuno-modulatory functions. The aim of this study is to use the rodent malaria model Plasmodium yoelii 17XL (P. y17XL) to examine whether pretreatment with ABPS will modulate host immunity against malaria infection and improve the outcome of the disease. METHODS: To determine whether ABPS could modulate immunity against malaria, mice were pretreated with ABPS prior to blood-stage infection by P. y17XL. Host survival and parasitaemia were monitored daily. The effect of pretreatment on host immune responses was studied through the quantitation of cytokines, dendritic cell populations, and natural regulatory T cells (Treg). RESULTS: Pretreatment with ABPS prior to infection significantly extended the survival time of mice after P. y17XL infection. At three and five days post-infection, ABPS pretreated mice developed stronger Th1 immune responses against malaria infection with the number of F4/80+CD36+ macrophages and levels of IFN-γ, TNF-α and nitric oxide being significantly higher than in the control group. More importantly, ABPS-treated mice developed more myeloid (CD11c+CD11b+) and plasmacytoid dendritic cells (CD11c+CD45R+/B220+) than control mice. ABPS pretreatment also resulted in modulated expression of MHC-II, CD86, and especially Toll-like receptor 9 by CD11c+ dendritic cells. In comparison, pretreatment with ABPS did not alter the number of natural Treg or the production of the anti-inflammatory cytokine IL-10. CONCLUSION: Pretreatment with the immuno-modulatory ABPS selectively enhanced Th1 immune responses to control the proliferation of malaria parasites, and prolonged the survival of mice during subsequent malaria infection.

Ultrasound microbubble-mediated delivery of ANLN silencing-repressed EZH2 expression alleviates cervical cancer progression.

Ultrasound-targeted microbubble destruction (UTMD) is a new gene therapy method that uses ultrasound and microbubbles carrying target genes to achieve gene transfection. However, whether UTMD-mediated ANLN silencing transfection helps to restrain the growth of cervical cancer (CC) is obscure. ANLN level in tumor tissues, adjacent tissues, and cells was tested using the database, qRT-PCR, and western blot. The optimal concentration of SF6 was determined by MTT assay. Mechanical index (MI) was selected by flow cytometry. After transfection with liposome or UTMD-mediated liposome, cell function experiments, qRT-PCR, and western blot were employed to assess CC cell biological behaviors and EZH2 level. Epithelial-mesenchymal transition (EMT)-related marker and apoptosis-related marker expressions were examined utilizing qRT-PCR and western blot. 10% SF6 and MI of 0.28 were selected for subsequent tests. ANLN was highly expressed in CC and cells. The transfection efficiency of the UTMD-siANLN group was higher than that of the L-siANLN group. Moreover, the repression of UTMD-siANLN on CC cell malignant phenotypes was stronger than L-siANLN. UTMD-siANLN attenuated EZH2 expression in CC cells. The modulatory role of UTMD-siANLN on EMT- and apoptosis-related markers was reversed by EZH2 overexpression. UTMD can improve the efficiency of siANLN transfection into CC cells to induce suppression of CC cell malignant phenotypes, which may become a new target of gene therapy for CC.

The Trend of Burn Injury Patients in Ningbo between 2012 and 2021: A Clinical Study.

Objective: This study was designed to understand the local changes of burn injuries in recent 10 years, so as to provide reliable reference data and viewpoints for prevention and vigilance of local burn injuries. Methods: In this study, 184 patients with a burn injury admitted to our hospital from 2012 to 2021 were enrolled and analyzed retrospectively. According to their information in the electronic database, the number of patients with burn injuries and the location of each disaster each year were analyzed, and the age, sex, hospital stay and hospitalization expense of each patient were collected. With 5 years as the boundary, the patients were divided into a 2012-2016 group and a 2017-2021 group and the differences of the two groups in the abovementioned aspects were compared. Results: During 2012-2021, the incidence rate of burn injuries in men was higher than that in women and workplaces had a higher burn injury rate than residents' homes. Compared with the period of 2012-2016, the number of fires or explosions and the number of patients with a burn injury during 2017-2028 both increased, but there was no significant change in disaster location, male-female ratio, age, average hospital stay, and average hospitalization expense. Conclusion: In the face of the increasing prevalence of burn injuries, we should strengthen fire-fighting knowledge-related education and fire prevention management and actively explore post-burn injury treatment strategies and potential treatment targets to promote the development of burn injury management and treatment strategies.

Use of Composite Acellular Dermal Matrix-Ultrathin Split-Thickness Skin in Hand Hot-Crush Injuries: A One-Step Grafting Procedure.

Background: Hot-crush injuries to the hands can be devastating, and early debridement and coverage with skin autograft remains the golden standard of wound treatment. However, this type of treatment is not feasible or unlikely to succeed due to limited donor sites and wound characteristics of hot-crush injuries on hands. Thus, the composite grafting of acellular dermal matrix (ADM) and split-thickness skin graft (STSG) as a novel alternative method has been attempted. In this series, the results are presented to demonstrate the feasibility and effectiveness of the use of one-stage procedure for early reconstruction in hand hot-crush injuries. Methods: All consecutive patients with hand hot-crush injuries, who underwent one-stage procedure of ADM and ultrathin STSG for soft tissue coverage at our institution from December 2018 to November 2019, were retrospectively analyzed. Wound dressings were opened on 7 days after operation to examine graft survival and complications. Patients were followed up for at least 9 months to evaluate their hand profiles. Results: Samples of 14 patients with a total of 23 wounds were involved in the study. Thirteen of the 23 third-fourth-degree wounds had varying degrees of tendon exposure. On 7 days postoperation, the composite grafts survived in 12 patients with minimal focal graft losses and liquefaction and necrosis in 2 patients, which achieved successful healing following new coverage of ultrathin STSG. All the wounds healed with hospital stays ranging from 9 days to 32 days (median: 24.5 days). At the final follow-up (from 9 months to 20 months), all patients achieved excellent or good total active motion grade and good scar quality (Vancouver scar scale scored 1-3) with no revision surgery. Conclusions: One-stage composite grafting of ADM and ultrathin STSG is a reliable alternative for early reconstruction in hand hot-crush injuries, which delivers good functional outcomes and a good cosmetic appearance.