Synthesis, characterization and irradiation enhances anticancer activity of liposome-loaded iridium(III) complexes.

Herein, we synthesized and characterized two novel iridium (III) complexes: [Ir(bzq)2(PPD)](PF6) (4a, with bzq = deprotonated benzo[h]quinoline and PPD = pteridino[6,7-f][1,10]phenanthroline-11,13-diamine) and [Ir(piq)2(PPD)](PF6) (4b, with piq = deprotonated 1-phenylisoquinoline). The anticancer efficacy of these complexes, 4a and 4b, was investigated using 3-(4,5-dimethylthiazole)-2,5-diphenltetraazolium bromide (MTT). Complex 4a exhibited no cytotoxic activity, while 4b demonstrated moderate efficacy against SGC-7901, A549, and HepG2 cancer cells. To enhance their anticancer potential, we explored two strategies: (I) light irradiation and (II) encapsulation of the complexes in liposomes, resulting in the formation of 4alip and 4blip. Both strategies significantly increased the ability of 4a, 4b to kill cancer cells. The cellular studies indicated that both the free complexes 4a, 4b and their liposomal forms 4alip and 4blip effectively inhibited cell proliferation. The cell cycle arrest analysis uncovered 4alip and 4blip arresting cell growth in the S period. Additionally, we investigated apoptosis and ferroptosis pathways, observing an increase in malondialdehyde (MDA) levels, a reduction of glutathione (GSH), a down-regulation of GPX4 (glutathione peroxidase) expression, and lipid peroxidation. The effects on mitochondrial membrane potential and intracellular Ca2+ concentrations were also examined, revealing that both light-activated and liposomal forms of 4alip and 4blip caused a decline in mitochondrial membrane potential and an enhancement in intracellular Ca2+ levels. In conclusion, these complexes and them encapsulated liposomes induce cell death through apoptosis and ferroptosis.

Case report: A 56-year-old woman presenting with torsades de pointes and cardiac arrest associated with levosimendan administration and underlying congenital long QT syndrome type 1.

Torsades de Pointes (TdP) is a malignant polymorphic ventricular tachycardia with heart rate corrected QT interval (QTc) prolongation, which may be attributed to congenital and acquired factors. Although various acquired factors for TdP have been summarized, levosimendan administration in complex postoperative settings is relatively uncommon. Timely identification of potential causes and appropriate management may improve the outcome. Herein, we describe the postoperative case of a 56-year-old female with initial normal QTc who accepted the administration of levosimendan for heart failure, suffered TdP, cardiac arrest, and possible Takotsubo cardiomyopathy, further genetically confirmed as long QT syndrome type 1 (LQT1). The patient was successfully treated with magnesium sulfate, atenolol, and implantable cardioverter defibrillator implantation. There should be a careful evaluation of the at-risk populations and close monitoring of the electrocardiograms, particularly the QT interval, to reduce the risk of near-fatal arrhythmias during the use of levosimendan.

Sodium-glucose cotransporter-2 inhibitors and the risk of lung cancer among patients with type 2 diabetes.

We sought to determine whether the use of sodium-glucose cotransporter-2 (SGLT-2) inhibitors is associated with a decreased risk of incident lung cancers among patients with type 2 diabetes. We assembled a new-user, active comparator cohort of SGLT-2 inhibitor and dipeptidyl peptidase-4 (DPP-4) inhibitor users using the United Kingdom Clinical Practice Research Datalink. We fit Cox proportional hazards models with propensity score fine stratification weighting to estimate hazard ratios (HRs) with 95% confidence intervals (CIs) for incident lung cancer. Crude incidence rates were 0.94 per 1000 person-years among 69 675 SGLT-2 inhibitor users followed for a median of 2.4 years and 1.45 per 1000 person-years among 151 495 DPP-4 inhibitor users followed for a median of 3.7 years. No reduced short-term risk of lung cancer was observed among SGLT-2 inhibitor users after weighting (HR 0.96, 95% CI 0.77-1.21). Further research with a longer follow-up period may be warranted.

Asperustins A-J: Austocystins with Immunosuppressive and Cytotoxic Activities from Aspergillus ustus NRRL 5856.

Ten new (1-10) and nine known (11-19) austocystins, along with four known anthraquinones (20-23), were isolated from the culture of Aspergillus ustus NRRL 5856 by bioactivity-guided fractionation. The structures of the new compounds were elucidated by spectroscopic data analysis, X-ray crystallographic study, the modified Mosher's method, [Rh2(OCOCF3)4]-induced ECD spectral analysis, and comparison of the experimental ECD spectra with those of the similar analogues. Compounds 1-8 represent the first examples of austocystins with a C-4' oxygenated substitution. The absolute configuration of 1″-hydroxy austocystin D (11) was determined by single-crystal X-ray diffraction and consideration of its biosynthetic origin. Compounds 5, 9, and 11 exhibited significant inhibitory effects against the proliferation of ConA-induced T cells with IC50 values of 1.1, 1.0, and 0.93 µM, respectively. Furthermore, these compounds suppressed the expression of IL-6 in a dose-dependent manner. Compounds 10-12 and 14 showed pronounced cytotoxicities against MCF-7 with IC50 values of 3.9, 1.3, 0.46, and 2.3 µM, respectively.

ß-Sitosterol attenuates anlotinib resistance in non-small cell lung cancer cells by inhibiting miR-181a-3p/SHQ1 signaling.

Anlotinib is used for the treatment of advanced non-small cell lung cancer; however, the emergence of drug resistance limits its clinical application. ß-sitosterol may also be used to treat lung cancer, but there have been no studies evaluating ß-sitosterol against anlotinib-resistant lung cancer. The purpose of this study was to determine the mechanism by which ß-sitosterol enhances the sensitivity of lung cancer cells to anlotinib. A549 cells were treated with different concentrations of anlotinib to generate anlotinib-resistant cells (A549/anlotinib cells). miR-181a-3p mimics were transfected into A549/anlotinib cells. A549 and A549/anlotinib cells were treated with ß-sitosterol at various concentrations. The Cell Counting Kit-8 (CCK-8) assay was used to measure cell proliferation. Apoptosis was assessed by flow cytometry. Real-time quantitative PCR was used to measure the expression of miR-181a-3p. The interaction of miR-181a-3p with the H/ACA ribonucleoprotein assembly factor (SHQ1) was predicted using the miRDB and TargetScan Human databases and verified with a luciferase reporter assay. The expression of SHQ1, activating transcription factor 6 (ATF6), and glucose-regulated protein 78 (GRP78) were measured by western blot analysis. ß-Sitosterol effectively suppressed A549/anlotinib cell proliferation and promoted apoptosis. SHQ1 is a downstream target of miR-181a-3p. The expression of miR-181a-3p was inhibited; however, SHQ1 expression was increased by ß-sitosterol treatment of A549/anlotinib cells. The inhibition of SHQ1, ATF6, and GRP78 protein expression by ß-sitosterol in A549/anlotinib cells was rescued by increased miR-181a-3p. ß-Sitosterol markedly promotes anlotinib-resistant A549 cell apoptosis and inhibits cell proliferation by activating SHQ1/UPR signaling through miR-181a-3p inhibition.

The effectiveness of a transtheoretical model-based smoking cessation intervention for rural smokers: A quasi-experimental longitudinal study.

OBJECTIVE: Cigarette smoking is highly prevalent, despite being a primary preventable cause of disease and mortality. This study examined the effect of a Transtheoretical Model (TTM)-based psychoeducational intervention for smoking cessation (SC) on knowledge, SC-related parameters, and progression through the TTM stages of change among rural smokers. METHODS: This quasi-experimental study recruited 200 smokers from an outpatient clinic. The comparison group was recruited before the experimental group to address possible self-selection bias. Structured questionnaires were administered pre- and post-intervention (three months) and at follow-up (six months). RESULTS: A generalised estimation equation model indicated that the TTM-based intervention significantly increased participants' SC-knowledge and improved progression through TTM stages by the six-month follow-up. No significant group differences were found in self-efficacy and nicotine dependence scores or daily cigarette consumption. CONCLUSIONS: A TTM-based intervention enhances SC-knowledge and fosters progress through change stages. However, it does not directly impact nicotine dependence or cigarette consumption. Outpatient settings may employ TTM-based programmes for SC education and motivation. Detecting anticipated effects may require a longer intervention duration exceeding six months. PRACTICE IMPLICATIONS: Such TTM-based programmes may facilitate SC-knowledge and motivation in outpatient settings. Further research to comprehend patients' context and experiences during the stages of change is required.

Myeloid-derived suppressor cells from tumour-bearing mice induce the population expansion of CD19hiFcγRIIbhi regulatory B cells via PD-L1.

Myeloid-derived suppressor cells (MDSCs) increase in number and gain immunosuppressive functions in tumours and many other pathological conditions. MDSCs are characterized by their strong T-cell immunosuppressive capacity. The effects that MDSCs may have on B cells, especially within the tumour microenvironment, are less well understood. Here, we report that either monocytic MDSCs or polymorphonuclear MDSCs can promote increases in interleukin (IL)-10-expressing CD19hiFcγRIIbhi regulatory B cells in vitro and in vivo. Splenic transitional-1, -2, and -3 cells and marginal zone B cells, but not follicular B cells, differentiate into IL-10-expressing CD19hiFcγRIIbhi regulatory B cells. The adoptive transfer of CD19hiFcγRIIbhi regulatory B cells via tail vein injection can promote subcutaneous 3LL tumour growth in mice. The expression of programmed death-ligand 1 on MDSCs was found to be strongly associated with CD19hiFcγRIIbhi regulatory B cell population expansion. Furthermore, the frequency of circulating CD19+FcγRIIhi regulatory B cells was significantly increased in advanced-stage lung cancer patients. Our results unveil a critical role of MDSCs in regulatory B-cell differentiation and population expansion in lung cancer patients.

Germline Mutations of Holliday Junction Resolvase Genes in Multiple Primary Malignancies Involving Lung Cancer Lead to PARP Inhibitor Sensitization.

PURPOSE: The incidence of multiple primary malignancies (MPM) involving lung cancer has increased in recent decades. There is an urgent need to clarify the genetic profile of such patients and explore more efficacious therapy for them. EXPERIMENTAL DESIGN: Peripheral blood samples from MPM involving patients with lung cancer were assessed by whole-exome sequencing (WES), and the identified variants were referenced for pathogenicity using the public available database. Pathway enrichment analysis of mutated genes was performed to identify the most relevant pathway. Next, the effects of mutations in relevant pathway on function and response to targeted drugs were verified by in vitro and in vivo experiments. RESULTS: Germline exomes of 71 patients diagnosed with MPM involving lung cancer were sequenced. Pathway enrichment analysis shows that the homologous recombination repair (HRR) pathway has the strongest correlation. Moreover, HRR genes, especially key Holliday junction resolvases (HJR) genes (GEN1, BLM, SXL4, and RMI1), were most frequently mutated, unlike the status in the samples from patients with lung cancer only. Next, we identified a total of seven mutations in HJR genes led to homologous recombination DNA repair deficiency and rendered lung cancer cells sensitive to PARP inhibitor treatment, both in vitro and in vivo. CONCLUSIONS: This is the first study to map the profile of germline mutations in patients with MPM involving lung cancer. This study may shed light on early prevention and novel targeted therapies for MPM involving patients with lung cancer with HJR mutations.

Enhanced Recovery after Surgery (ERAS) in Postoperative Lung Cancer Patients: A Novel Perioperative Strategy for Preventing Venous Thromboembolism and Improving Quality of Life.

This study aimed to assess the impact of enhanced recovery after surgery (ERAS) intervention in preventing venous thromboembolism (VTE) among postoperative lung cancer patients. Conducted from January 2022 to January 2023, the research involved 125 lung cancer patients randomly assigned to either a control group (n = 60) receiving routine care, or an ERAS group (n = 65) which received both routine care and ERAS interventions. The ERAS program comprised a comprehensive series of interventions meticulously implemented throughout the preoperative, intraoperative, and postoperative phases. Thrombotic risk assessment using the Caprini Risk Assessment Model (RAM) was conducted preoperatively and on postoperative day 5 (POD 5), with plasma D-dimer levels measured preoperatively, on POD 1, POD 3, and POD 5. Quality of life and patient satisfaction were assessed at discharge using the European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Questionnaire-Lung Cancer Module 13 (QLQ-LC13) and The Newcastle Satisfaction with Nursing Scale (NSNS), respectively. The ERAS group demonstrated significantly lower Caprini RAM scores on POD 5 compared to the control group, with lower D-dimer levels on POD 3 and POD 5. The incidence of VTE was lower in the ERAS group (1.54%) compared to the control group (11.67%) during hospitalization. At discharge, the ERAS group showed improved quality of life, with higher satisfaction scores for nursing care and their hospital stay. ERAS nursing interventions effectively mitigate thrombotic risk, improve D-dimer levels, enhance postoperative quality of life, and elevate patient satisfaction among individuals undergoing lung cancer surgery.

Clinical and Immunological Significance of ANKRD52 in Pan-Cancer.

Ankyrin repeat domain 52 (ANKRD52) is a regulatory component of the protein phosphatase 6 (PP6) holoenzyme. Evidence has emerged to suggest involvement of ANKRD52 in tumor metastases and cancer cell escape from T cell-mediated elimination and immunotherapy but there has been no research across different cancer types. The current study explored the biological functions of ANKRD52 by combining data from many databases. The aim was to expose new diagnostic or treatment biomarkers for malignant tumors. The roles of ANKRD52 with respect to immunotherapy in 33 human cancer types were analyzed by combining data from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx), Cancer Cell Line Encyclopedia (CCLE), UCSC Xena, the Tumor Immune Estimation Resource (TIMER), TISIDB and Cellminer. Bioinformatics methods were used to analyze the association between ANKRD52 expression and prognosis, immunological indicators (immune cell infiltration, ESTIMATE scores and tumor microenvironment (TME) signatures), tumor mutational burden (TMB), microsatellite instability (MSI) and drug sensitivity. ANKRD52 expression was generally higher in 24 tumor tissues than in normal tissues and was associated with poor prognosis, especially in kidney chromophobe (KICH). Lower expression was observed in advanced cancer. ANKRD52 expression was strongly linked to major immunological indicators, such as immune cell infiltration, ESTIMATE scores, TME signatures, as well as expression of immune and tumor-related genes. Expression was also associated with indicators of immunotherapy efficacy and outcome, such as TMB in 7 cancer types and MSI in 12. In addition, ANKRD52 expression was linked to sensitivity to a number of anticancer drugs. ANKRD52 had a distinct immune function in breast invasive carcinoma (BRCA) that correlated negatively with most immune indicators. Expression was enriched in proliferation-, differentiation- and metabolism-related pathways and linked to other immune cells and TME signatures. A nomogram to predict 3- or 5-year overall survival (OS) of patients with BRCA was constructed. ANKRD52 may have utility as an oncological and immunological biomarker. New insights into oncogenesis are presented and the development of ANKRD52-targeting to increase the therapeutic efficacy of immunotherapy combined with chemotherapy explored.

Characteristics of iron (hydr)oxides and Cr(VI) retention mechanisms in soils from tropical and subtropical areas of China.

Though both iron (hydr)oxides and soil organic matter (SOM) significantly influence heavy metal behaviors in soils, studies on the characteristics of natural minerals and the synergic effects of the two on Cr(VI) transformation are limited. This study investigated Cr(VI) retention mechanisms in four soils from tropical and subtropical regions of China based on a comprehensive characterization of Fe (hydr)oxides. These soils exhibited varying quantities of hematite, ferrihydrite and goethite, with distinct Al substitution levels and varied exposed crystallographic facets. Adsorption experiments revealed a positive correlation between Fe (hydr)oxide content and Cr(VI) fixation amount on colloid, which was influenced by the mineral types, Al substitution levels and facet exposures. Further, Cr(VI) was sequestered on soil by adsorption and reduction. In soils enriched with crystalline Fe (hydr)oxides, Cr(VI) reduction was primarily governed by SOM, while in soils enriched with poorly crystalline Fe (hydr)oxides, mineral-associated Fe(II) also contributed to Cr(VI) reduction. Aging experiments demonstrated that SOM and mineral-associated Fe(II) expedited Cr (VI) passivation and diminished the Cr leaching. These results improve our understanding of natural Fe (hydr)oxide structures and their impact on Cr(VI) behavior in soils, and shed light on complex soil-contaminant interactions and remediation of Cr(VI) polluted soils.

Synergistic anticancer effect by targeting CDK2 and EGFR-ERK signaling.

The EGFR-RAS-ERK pathway is one of the most important signaling cascades in cell survival, growth, and proliferation. Aberrant activation of this pathway is a common mechanism in various cancers. Here, we report that CDK2 is a novel regulator of the ERK pathway via USP37 deubiquitinase (DUB). Mechanistically, CDK2 phosphorylates USP37, which is required for USP37 DUB activity. Further, USP37 deubiquitinates and stabilizes ERK1/2, thereby enhancing cancer cell proliferation. Thus, CDK2 is able to promote cell proliferation by activating USP37 and, in turn, stabilizing ERK1/2. Importantly, combined CDK1/2 and EGFR inhibitors have a synergetic anticancer effect through the downregulation of ERK1/2 stability and activity. Indeed, our patient-derived xenograft (PDX) results suggest that targeting both ERK1/2 stability and activity kills cancer cells more efficiently even at lower doses of these two inhibitors, which may reduce their associated side effects and indicate a potential new combination strategy for cancer therapy.

Metabolic regulation of homologous recombination repair by MRE11 lactylation.

Lactylation is a lactate-induced post-translational modification best known for its roles in epigenetic regulation. Herein, we demonstrate that MRE11, a crucial homologous recombination (HR) protein, is lactylated at K673 by the CBP acetyltransferase in response to DNA damage and dependent on ATM phosphorylation of the latter. MRE11 lactylation promotes its binding to DNA, facilitating DNA end resection and HR. Inhibition of CBP or LDH downregulated MRE11 lactylation, impaired HR, and enhanced chemosensitivity of tumor cells in patient-derived xenograft and organoid models. A cell-penetrating peptide that specifically blocks MRE11 lactylation inhibited HR and sensitized cancer cells to cisplatin and PARPi. These findings unveil lactylation as a key regulator of HR, providing fresh insights into the ways in which cellular metabolism is linked to DSB repair. They also imply that the Warburg effect can confer chemoresistance through enhancing HR and suggest a potential therapeutic strategy of targeting MRE11 lactylation to mitigate the effects.

Integrative pharmacology reveals the mechanisms of Erzhi pills, A traditional Chinese formulation, stimulating melanogenesis.

ETHNOPHARMACOLOGICAL RELEVANCE: Erzhi pills (EZP), a traditional Chinese medicine formula prescribed for the treatment of vitiligo, has shown promising efficacy. However, the oral bioactive components and mechanisms underlying the promotion of melanogenesis by EZP remain unclear. AIM OF THE STUDY: This study aimed to investigate the pharmacological basis and mechanism of EZP in promoting melanogenesis. MATERIALS AND METHODS: UHPLC-TOF-MS analysis was used to identify absorbed phytochemicals in serum after oral administration of EZP. Network pharmacology methods were used to predict potential targets and pathways involved in the melanogenic activity of EZP, resulting in the construction of a "compound-target-pathway" network. Zebrafish and B16F10 cells were used to evaluate the effects of EZP on tyrosinase activity and melanin content. Western blot and ELISA analyses were used to validate the effects of EZP on melanogenesis-related proteins, including MITF, TYR, CREB, p-CREB, and cAMP. RESULTS: UHPLC-TOF-MS analysis identified 36 compounds derived from EZP in serum samples. Network pharmacology predictions revealed 89 target proteins associated with the identified compounds and closely related to vitiligo. GO and KEGG analyses indicated the involvement of the cAMP/PKA signaling pathway in the promotion of melanogenesis by EZP. Experimental results showed that EZP increased tyrosinase activity and melanin content in zebrafish and B16F10 cells without inducing toxicity. Western blot and ELISA results suggested that the melanogenic effect of EZP may be related to the activation of the cAMP/PKA signaling pathway. These results confirm the feasibility of combining serum pharmacological and network pharmacological approaches. CONCLUSIONS: EZP have the potential to increase tyrosinase activity and melanin content in zebrafish and cells possibly through activation of the cAMP/PKA pathway.

Retraction: ET-1 promotes the growth and metastasis of esophageal squamous cell carcinoma via activating PI3K/Akt pathway.

[This retracts the article DOI: 10.21037/tcr.2020.04.26.].

Retraction Notice to: TNFAIP8 Promotes Cisplatin Chemoresistance in Triple-Negative Breast Cancer by Repressing p53-Mediated miR-205-5p Expression.

[This retracts the article DOI: 10.1016/j.omtn.2020.09.025.].

Radio- and Photosensitizing Os(II)-Based Nanocage for Combined Radio-/Chemo-/X-ray-Induced Photodynamic Therapies, NIR Imaging, and Drug Delivery.

Integration of clinical imaging and collaborative multimodal therapies into a single nanomaterial for multipurpose diagnosis and treatment is of great interest to theranostic nanomedicine. Here, we report a rational design of a discrete Os-based metal-organic nanocage Pd6(OsL3)828+ (MOC-43) as a versatile theranostic nanoplatform to meet the following demands simultaneously: (1) synergistic treatments of radio-, chemo-, and X-ray-induced photodynamic therapies (X-PDT) for breast cancer, (2) NIR imaging for cancer cell tracking and tumor-targeting, and (3) anticancer drug transport through a host-guest strategy. The nanoscale MOC-43 incorporates high-Z Os-element to interact with X-ray irradiation for dual radiosensitization and photosensitization, showing efficient energy transfer to endogenous oxygen in cancer cells to enhance X-PDT efficacy. It also features intrinsic NIR emission originating from metal-to-ligand charge transfer (MLCT) as an excellent imaging probe. Meanwhile, its 12 pockets can capture and concentrate low-water-soluble molecules for anticancer drug delivery. These multifunctions are implemented and demonstrated by micellization of coumarin-loaded cages with DSPE-PEG2000 into coumarin ⊂ MOC-43 nanoparticles (CMNPs) for efficient subcellular endocytosis and uptake. The cancer treatments in vitro/in vivo show promising antitumor performance, providing a conceptual protocol to combine cage-cargo drug transport with diagnosis and treatment for collaborative cancer theranostics by virtue of multifunction synergism on a single-nanomaterial platform.

Clinical study of acupuncture combined with surface anesthesia using proparacaine in geriatric cataract phacoemulsification.

BACKGROUND: During anesthesia administration for cataract surgery, low pH of proparacaine may induce pain or complications such as corneal damage and poor wound healing, with the use of additional drops intraoperatively increasing the risk of complications. Accordingly, there is a clinical need for adjuncts to local anesthesia needs to improve the efficiency of anesthesia and reduce the required amount of intraoperative proparacaine. AIM: To identify a method of anesthesia for geriatric cataract phacoemulsification that provides more efficient analgesia and improves clinical efficacy. METHODS: A total of 130 geriatric patients with cataracts who attended Hebei Eye Hospital from December 2020 to December 2022 were included in the present study. Patients were divided into the proparacaine surface anesthesia (SA) group (65 cases) and the compound acupuncture-medicine anesthesia group (CAMA group, 65 cases). Patients in the CAMA group were provided acupuncture analgesia in addition to SA. Preoperative anxiety [Self-Rating Anxiety Scale (SAS) score and state anxiety inventory (SAI) score], intraoperative stress, vital signs, analgesia, and cooperation, as well as postoperative adverse events, were compared between groups. RESULTS: More marked reductions in anxiety were observed among patients in the CAMA group, with corresponding reductions in SAS and SAI scores. During the operation, no change in the secretion of E, NE, or Cor group compared to the preoperative period was observed in the CAMA, which was markedly lower than that in the SA group. Heart rate, blood pressure, and respiratory rate were more stable intraoperatively in the CAMA group. In addition, the incidence of intraoperative pain and the number of additional doses of anesthesia required in the CAMA group were markedly lower than in the SA group. Accordingly, patients in the CAMA group were able to avoid eye movements and eyelid closing leading to greater cooperation with surgeons during surgery. Furthermore, marked reductions in intraoperative adverse effects were observed in the CAMA group, indicating greater overall safety. CONCLUSION: Proparacaine SA combined with acupuncture as an analgesic provides improved analgesia with greater safety compared to surface anesthesia with proparacaine during geriatric cataract phacoemulsification.

Solutions for an efficient arsenite oxidation and removal from groundwater containing ferrous iron.

Manganese (Mn) oxides are extensively used to oxidize As(III) present in ground, drinking, and waste waters to the less toxic and more easily removable As(V). The common presence of multiple other cations in natural waters, and more especially of redox-sensitive ones such as Fe2+, may however significantly hamper As(III) oxidation and its subsequent removal. The present work investigates experimentally the influence of Mn(III) chelating agents on As(III) oxidation process in such environmentally relevant complex systems. Specifically, the influence of sodium pyrophosphate (PP), an efficient Mn(III) chelating agent, on As(III) oxidation by birnessite in the presence of Fe(II) was investigated using batch experiments at circum-neutral pH. In the absence of PP, competitive oxidation of Fe(II) and As(III) leads to Mn oxide surface passivation by Fe(III) and Mn(II/III) (oxyhydr)oxides, thus inhibiting As(III) oxidation. Addition of PP to the system highly enhances As(III) oxidation by birnessite even in the presence of Fe(II). PP presence prevents passivation of Mn oxide surfaces keeping As and Fe species in solution while lower valence Mn species are released to solution. In addition, reactive oxygen species (ROS), tentatively identified as hydroxyl radicals (•OH), are generated under aerobic conditions through oxygen activation by Fe(II)-PP complexes, enhancing As(III) oxidation further. The positive influence of Mn(III) chelating agents on As(III) oxidation most likely not only depend on their affinity for Mn(III) but also on their ability to promote formation of these active radical species. Finally, removal of As(V) through sorption to Fe (oxyhydr)oxides is efficient even in the presence of significant concentrations of PP, and addition of such Mn(III) chelating agents thus appears as an efficient way to enhance the oxidizing activity of birnessite in large-scale treatment for arsenic detoxification of groundwaters.

Surgical correction of Tessier cleft no. 7: A single center 18-year experience.

INTRODUCTION: Tessier cleft 7 are rare craniofacial clefts. Live-birth incidence varies from 1/80,000 to 1/300,000, with the incidence of 1 in 120 craniofacial clefts among Asians. Its clinical presentation varies widely in severity, thus, complicating diagnosis and contributing to the lack of consensus regarding its surgical management. The aim of this study is to describe clinical findings, types of Tessier cleft 7 soft tissue repair, and its outcomes in Kuala Lumpur Hospital. METHODS: This retrospective study reviewed records of children operated from January 2001 to July 2019. Data regarding concurrent congenital anomalies, complications, type of surgery, etc., were collected from outpatient records, operative notes, and clinical photographs. RESULTS: Twenty-eight children were treated, and 33 clefts (5 bilateral) were repaired. The male-to-female ratio was 1.3:1 (16 males and 12 females). Twenty-three patients had unilateral clefts (82.14%), with 14 right (60.86%) and 8 left (34.78%). Bilateral clefts were less common (17.86%). Twenty-three patients (82.14%) were Malay, 3 (10.71%) Chinese, 1 (3.57%) Indian, and 1 (3.57%) Cambodian. Eleven medical records were untraceable (discontinued due to duration of inactivity). There were 10 straight-line repairs, 5 Z-plasties, and 1 W-plasty performed; 3 cases did not detail the type of repair. One child required scar revision, and 1 had hypertrophic scarring requiring corticosteroid injection-no disturbances in speech or oral incompetency while eating were reported. Duration of follow-up ranged from 3 to 14 years. CONCLUSION: Our center has a higher rate of Tessier cleft 7 attendance. Straight-line cutaneous repairs combined with inferior vermilion mucosal flap can be used with low rates of complication and revision surgery.