Homoharringtonine Inhibits the NOTCH/MYC Pathway and Exhibits Anti-Tumor Effects in T-Cell Acute Lymphoblastic Leukemia.

We report on the antileukemic activity of homoharringtonine (HHT) in T-ALL. We showed that HHT inhibited NOTCH/MYC pathway and induced a significantly longer survival in T-ALL mouse and patient-derived xenograft models, therefore supporting HHT as a promising agent for T-ALL.

Novel TFG mutation causes autosomal-dominant spastic paraplegia and defects in autophagy.

BACKGROUND: Mutations in the tropomyosin receptor kinase fused (TFG) gene are associated with various neurological disorders, including autosomal recessive hereditary spastic paraplegia (HSP), autosomal dominant hereditary motor and sensory neuropathy with proximal dominant involvement (HMSN-P) and autosomal dominant type of Charcot-Marie-Tooth disease type 2. METHODS: Whole genome sequencing and whole-exome sequencing were used, followed by Sanger sequencing for validation. Haplotype analysis was performed to confirm the inheritance mode of the novel TFG mutation in a large Chinese family with HSP. Additionally, another family diagnosed with HMSN-P and carrying the reported TFG mutation was studied. Clinical data and muscle pathology comparisons were drawn between patients with HSP and patients with HMSN-P. Furthermore, functional studies using skin fibroblasts derived from patients with HSP and patients with HMSN-P were conducted to investigate the pathomechanisms of TFG mutations. RESULTS: A novel heterozygous TFG variant (NM_006070.6: c.125G>A (p.R42Q)) was identified and caused pure HSP. We further confirmed that the well-documented recessively inherited spastic paraplegia, caused by homozygous TFG mutations, exists in a dominantly inherited form. Although the clinical features and muscle pathology between patients with HSP and patients with HMSN-P were distinct, skin fibroblasts derived from both patient groups exhibited reduced levels of autophagy-related proteins and the presence of TFG-positive puncta. CONCLUSIONS: Our findings suggest that autophagy impairment may serve as a common pathomechanism among different clinical phenotypes caused by TFG mutations. Consequently, targeting autophagy may facilitate the development of a uniform treatment for TFG-related neurological disorders.

MicroRNA networks in FLT3-ITD acute myeloid leukemia.

MiR-126 and miR-155 are key microRNAs (miRNAs) that regulate, respectively, hematopoietic cell quiescence and proliferation. Herein we showed that in acute myeloid leukemia (AML), the biogenesis of these two miRNAs is interconnected through a network of regulatory loops driven by the FMS-like tyrosine kinase 3-internal tandem duplication (FLT3-ITD). In fact, FLT3-ITD induces the expression of miR-155 through a noncanonical mechanism of miRNA biogenesis that implicates cytoplasmic Drosha ribonuclease III (DROSHA). In turn, miR-155 down-regulates SH2-containing inositol phosphatase 1 (SHIP1), thereby increasing phosphor-protein kinase B (AKT) that in turn serine-phosphorylates, stabilizes, and activates Sprouty related EVH1 domain containing 1 (SPRED1). Activated SPRED1 inhibits the RAN/XPO5 complex and blocks the nucleus-to-cytoplasm transport of pre-miR-126, which cannot then complete the last steps of biogenesis. The net result is aberrantly low levels of mature miR-126 that allow quiescent leukemia blasts to be recruited into the cell cycle and proliferate. Thus, miR-126 down-regulation in proliferating AML blasts is downstream of FLT3-ITD­dependent miR-155 expression that initiates a complex circuit of concatenated regulatory feedback (i.e., miR-126/SPRED1, miR-155/human dead-box protein 3 [DDX3X]) and feed-forward (i.e., miR-155/SHIP1/AKT/miR-126) regulatory loops that eventually converge into an output signal for leukemic growth.

Clinical, pathological and genetic features and follow-up of 110 patients with late-onset MADD: a single-center retrospective study.

To observe a long-term prognosis in late-onset multiple acyl-coenzyme-A dehydrogenation deficiency (MADD) patients and to determine whether riboflavin should be administrated in the long-term and high-dosage manner, we studied the clinical, pathological and genetic features of 110 patients with late-onset MADD in a single neuromuscular center. The plasma riboflavin levels and a long-term follow-up study were performed. We showed that fluctuating proximal muscle weakness, exercise intolerance and dramatic responsiveness to riboflavin treatment were essential clinical features for all 110 MADD patients. Among them, we identified 106 cases with ETFDH variants, 1 case with FLAD1 variants and 3 cases without causal variants. On muscle pathology, fibers with cracks, atypical ragged red fibers (aRRFs) and diffuse decrease of SDH activity were the distinctive features of these MADD patients. The plasma riboflavin levels before treatment were significantly decreased in these patients as compared to healthy controls. Among 48 MADD patients with a follow-up of 6.1 years on average, 31 patients were free of muscle weakness recurrence, while 17 patients had episodes of slight muscle weakness upon riboflavin withdrawal, but recovered after retaking a small-dose of riboflavin for a short-term. Multivariate Cox regression analysis showed vegetarian diet and masseter weakness were independent risk factors for muscle weakness recurrence. In conclusion, fibers with cracks, aRRFs and diffuse decreased SDH activity could distinguish MADD from other genotypes of lipid storage myopathy. For late-onset MADD, increased fatty acid oxidation and reduced riboflavin levels can induce episodes of muscle symptoms, which can be treated by short-term and small-dose of riboflavin therapy.

Seed germination demonstrates inter-annual variations in alkaline tolerance: a case study in perennial Leymus chinensis.

BACKGROUND AND AIMS: The escalating issue of soil saline-alkalization poses a growing global challenge. Leymus chinensis is a perennial grass species commonly used in the establishment and renewal of artificial grasslands that is relatively tolerant of saline, alkaline, and drought conditions. Nonetheless, reduced seed setting rates limit its propagation, especially on alkali-degraded grassland. Inter-annual variations have an important effect on seed yield and germination under abiotic stress, and we therefore examined the effect of planting year on seed yield components of L. chinensis. METHODS: We grew transplanted L. chinensis seedlings in pots for two (Y2), three (Y3), or four (Y4) years and collected spikes for measurement of seed yield components, including spike length, seed setting rate, grain number per spike, and thousand seed weight. We then collected seeds produced by plants from different planting years and subjected them to alkaline stress (25 mM Na2CO3) for measurement of germination percentage and seedling growth. RESULTS: The seed setting rate of L. chinensis decreased with an increasing number of years in pot cultivation, but seed weight increased. Y2 plants had a higher seed setting rate and more grains per spike, whereas Y4 plants had a higher thousand seed weight. The effects of alkaline stress (25 mM Na2CO3) on seed germination were less pronounced for the heavier seeds produced by Y4 plants. Na2CO3 caused a 9.2% reduction in shoot length for seedlings derived from Y4 seeds but a 22.3% increase in shoot length for seedlings derived from Y3 seeds. CONCLUSIONS: Our findings demonstrate significant differences in seed yield components among three planting years of L. chinensis under pot cultivation in a finite space. Inter-annual variation in seed set may provide advantages to plants. Increased alkalinity tolerance of seed germination was observed for seeds produced in successive planting years.

Lysosomal dysfunction and overload of nucleosides in thymidine phosphorylase deficiency of MNGIE.

Inherited deficiency of thymidine phosphorylase (TP), encoded by TYMP, leads to a rare disease with multiple mitochondrial DNA (mtDNA) abnormalities, mitochondrial neurogastrointestinal encephalomyopathy (MNGIE). However, the impact of TP deficiency on lysosomes remains unclear, which are important for mitochondrial quality control and nucleic acid metabolism. Muscle biopsy tissue and skin fibroblasts from MNGIE patients, patients with m.3243 A > G mitochondrial encephalopathy, lactic acidosis and stroke-like episodes (MELAS) and healthy controls (HC) were collected to perform mitochondrial and lysosomal functional analyses. In addition to mtDNA abnormalities, compared to controls distinctively reduced expression of LAMP1 and increased mitochondrial content were detected in the muscle tissue of MNGIE patients. Skin fibroblasts from MNGIE patients showed decreased expression of LAMP2, lowered lysosomal acidity, reduced enzyme activity and impaired protein degradation ability. TYMP knockout or TP inhibition in cells can also induce the similar lysosomal dysfunction. Using lysosome immunoprecipitation (Lyso- IP), increased mitochondrial proteins, decreased vesicular proteins and V-ATPase enzymes, and accumulation of various nucleosides were detected in lysosomes with TP deficiency. Treatment of cells with high concentrations of dThd and dUrd also triggers lysosomal dysfunction and disruption of mitochondrial homeostasis. Therefore, the results provided evidence that TP deficiency leads to nucleoside accumulation in lysosomes and lysosomal dysfunction, revealing the widespread disruption of organelles underlying MNGIE.

A comparative study on riboflavin responsive multiple acyl-CoA dehydrogenation deficiency due to variants in FLAD1 and ETFDH gene.

Lipid storage myopathy (LSM) is a heterogeneous group of lipid metabolism disorders predominantly affecting skeletal muscle by triglyceride accumulation in muscle fibers. Riboflavin therapy has been shown to ameliorate symptoms in some LSM patients who are essentially concerned with multiple acyl-CoA dehydrogenation deficiency (MADD). It is proved that riboflavin responsive LSM caused by MADD is mainly due to ETFDH gene variant (ETFDH-RRMADD). We described here a case with riboflavin responsive LSM and MADD resulting from FLAD1 gene variants (c.1588 C > T p.Arg530Cys and c.1589 G > C p.Arg530Pro, FLAD1-RRMADD). And we compared our patient together with 9 FLAD1-RRMADD cases from literature to 106 ETFDH-RRMADD cases in our neuromuscular center on clinical history, laboratory investigations and pathological features. Furthermore, the transcriptomics study on FLAD1-RRMADD and ETFDH-RRMADD were carried out. On muscle pathology, both FLAD1-RRMADD and ETFDH-RRMADD were proved with lipid storage myopathy in which atypical ragged red fibers were more frequent in ETFDH-RRMADD, while fibers with faint COX staining were more common in FLAD1-RRMADD. Molecular study revealed that the expression of GDF15 gene in muscle and GDF15 protein in both serum and muscle was significantly increased in FLAD1-RRMADD and ETFDH-RRMADD groups. Our data revealed that FLAD1-RRMADD (p.Arg530) has similar clinical, biochemical, and fatty acid metabolism changes to ETFDH-RRMADD except for muscle pathological features.

Skeletal muscle involvement in systemic amyloidosis is often overlooked.

AIM: Systemic amyloidosis is a condition in which misfolded amyloid fibrils are deposited within tissues. Amyloid myopathy is a rare manifestation of systemic amyloidosis. However, whether skeletal muscle involvement is underestimated and whether such deposition guarantees clinical and pathological myopathic features remain to be investigated. METHODS: We retrospectively reviewed patients with systemic amyloidosis, in whom skeletal muscle biopsies were performed at our centre between January 2018 and June 2023. In total, 28 patients with suspected systemic amyloidosis were included. Among these, 21 presented with cardiomyopathy but lacked myopathic symptoms. The clinical and pathological data of these patients were further analysed. The amyloid type was confirmed by immunohistochemistry. RESULTS: Twenty-eight patients with suspected systemic amyloidosis underwent muscle biopsy. Amyloid deposition in the skeletal muscle was confirmed in 24 patients, including 22 with light-chain amyloidosis (AL) and two with transthyretin amyloidosis (ATTR). Among the 24 patients, seven presented with muscle weakness and decreased muscle strength (Group 1, symptomatic myopathy), whereas the remaining 17 exhibited normal muscle strength (Group 2, asymptomatic myopathy). Group 1 included four patients with AL-λ, one with AL-κ and two with ATTR. Group 2 included 15 patients with AL-λ and two patients with AL-κ. In Group 1, six patients exhibited neuropathy, whereas only one patient in Group 2 presented with subclinical neuropathy on nerve conduction studies. Amyloid deposition in the interstitium was the most obvious change, observed in all 24 patients. Neuropathic changes, including denervation atrophy and muscle fibre grouping, were also common. Except for type 2 fibre atrophy, the other myopathic changes were mild and nonspecific. No sarcolemmal disruption was observed. Immunohistochemical analysis revealed marked positivity for MAC and MHC1 expression in the regions with amyloid deposits. Clinicopathological analysis revealed no significant differences in the extent of muscular amyloid deposition between the two groups. Nevertheless, patients in Group 1 displayed more pronounced neurogenic atrophy on skeletal muscle biopsies. CONCLUSIONS: Our study indicates that amyloid deposition in skeletal muscle is commonly observed but rarely causes symptomatic myopathy in systemic amyloidosis.

Ti4+ Ions-Doped Metal-Organic Framework (MOF-74) for Photoreduction of Carbon Dioxide.

The development of efficient and sustainable methods for reducing carbon dioxide (CO2) and converting it into valuable hydrocarbons has gained significant attention. In this study, researchers focused on Ti4+-doped metal-organic framework (MOF-74) photocatalysts. The incorporation of Ti4+ ions into the MOF-74 structure was achieved through a one-pot hydrothermal method. By replacing Zn2+ ions with Ti4+ ions in a substitutional manner, researchers have aimed to enhance the photocatalytic activity of the CO2 reduction. The obtained Ti4+-doped MOF-74 photocatalysts exhibited a significantly improved performance in the reduction of CO2 into carbon monoxide (CO). The doping of Ti4+ ions induced energy bands below the conduction band minimum (CBM) of MOF-74, extending the visible response range and enabling the photocatalysts to utilize a broader spectrum of light for catalytic reactions. This extension of the visible response range enables photocatalysts to utilize a broader spectrum of light for catalytic reactions. The incorporation of Ti4+ ions not only extends the visible response range but also suppresses charge carrier recombination. This work provides valuable insights into the design principles of MOF-based photocatalysts and paves the way for their practical implementation in addressing the energy crisis and reducing greenhouse gas emissions.

Doping strategies for inorganic lead-free halide perovskite solar cells: progress and challenges.

In recent years, remarkable advancements have been achieved in the field of halide perovskite solar cells (PSCs). However, the commercialization of PSCs has been impeded by challenges such as Pb leakage and the instability of hybrid organic-inorganic perovskites (HOIPs). Hence, the future lies in the development of environmentally friendly inorganic lead-free halide perovskites (LFHPs) based on elements like Sn, Ge, Bi, Sb, and Cu, which show great promise for photovoltaic applications. However, LFHP photovoltaic cells still face challenges such as low efficiency, poor film quality, and stability in comparison to HOIPs. These limitations significantly hinder their further development. To address these issues, element doping strategies, including cationic and anionic doping, as well as the use of additives, are frequently employed. These strategies aim to improve film quality, passivate defects, reduce the band gap, and enhance device performance and stability. In this paper, we aim to provide a comprehensive review of the recent research progress in doping strategies for LFHPs.

Spontaneous recovery in random hypergraphs.

In many real-world phenomena, such as the reconstruction of disaster areas after an earthquake or the stock market's recovery after an economic crisis, damaged networks are spontaneously active after receiving assistance. To reveal how the recovery process, the research of dynamic network recovery has become a hot topic in the field of network science. Previous studies on network recovery have been limited to simple networks with pairwise interactions. However, real-world systems are usually networks with higher-order interactions that are composed of multiple units. To better understand the recovery phenomenon on complex networks in the real world, we propose a novel spontaneous recovery model applied to hypergraphs. The model considers two types of recovery, internal recovery and fast recovery, where inactive nodes in the network can either recover internally with independent probabilities or receive sufficient resources from the hyperedge for fast recovery. We find that the number of active nodes in the system shows a phase change from continuous to discontinuous as the fast recovery condition is relaxed. Moreover, under the influence of higher-order interactions, increasing both average hyperedge cardinality and network heterogeneity contribute to increasing the network resilience. These findings help us understand the recovery mechanisms of complex networks and provide essential insights into designing highly resilient systems.

Household Environments and Cognitive Decline Among Middle-Aged and Older Adults in China: Exploring Gender, Age, and Residential Variations.

This study examined the relationship between household environments and trajectories of cognitive function among middle-aged and older adults in China and its urban/rural, gender, and age variations. We estimated multi-level linear growth curve models using a representative sample of 16,111 respondents aged 45 years and over from the China Health and Retirement Longitudinal Study (2011-2018). Older people who lived with a spouse, but not with children, and those with higher living expenditures, better housing quality, and indoor clean fuels for cooking had a slower cognitive decline. Living arrangement more strongly predicted men's cognitive decline, while living expenditure, solid fuel use, and housing quality significantly predicted only women's cognitive decline. Only for older adults and rural residents, those living alone had significantly faster cognitive decline than those living with a spouse only. These findings underscore the importance of improving the living conditions of older adults to help alleviate their cognitive decline.

End-stage renal disease in a critical patient with superior vena cava syndrome with central vein catheters inserted via the superficial femoral vein: A case study.

Superior vena cava syndrome (SVCS) is caused by obstruction to the blood flow through this vein. Indwelling central venous devices, such as cardiac pacemakers and haemodialysis catheters have emerged as the most common benign aetiology of SVCS. SVCS is particularly severe in patients with end-stage renal disease who require continuous renal replacement therapy plus infusion therapy. The presence of SVCS results in a reduction of available venous access for affected patients. Therefore, venous access plays a crucial role in the management of these patients. The importance of dealing with vascular access (VA) in critical patients with these conditions cannot be overstated. This case describes an 81-year-old man with respiratory failure who had end-stage renal disease complicated with SVCS. Using ultrasound-guided puncture, we inserted a peripherally inserted central catheter (PICC) into the superficial femoral vein to meet his infusion requirements in intensive care. After successful placement, the catheter tip position was adjusted using imaging to position the tip relative to the haemodialysis catheter. Whenever patients with severe renal dysfunction are treated, central veins should be preserved. Safe PICC access is possible via the superficial femoral vein to protect the last central VA for rational use. This meets urgent needs for infusion and deserves promotion.

Association of KMT2C/D loss-of-function variants with response to immune checkpoint blockades in colorectal cancer.

Immune checkpoint inhibitors (ICIs) have become important treatment strategies, yet responses vary among patients and predictive biomarkers are urgently needed. Mutations in KMT2C and KMT2D lead to increased levels of genomic instability. Therefore, we aimed to examine whether KMT2C/D mutations might be a predictor of immunotherapeutic efficacy. Here, we investigated the associations of KMT2C/D loss-of-function (LOF) variants with tumor mutation burden (TMB), MSI-H, PD-L1 expression, the levels of tumor-infiltrating leukocytes (TILs), and clinical response to ICIs. It was found that KMT2C/D LOF variants were associated with higher TMB. Compared with the non-LOF group, the proportion of patients with MSI-H tumors was larger in the LOF group. PD-L1 expression was higher in the LOF group only for colorectal cancer in both the Chinese and The Cancer Genome Atlas cohorts. Importantly, KMT2C/D LOF variants were associated with decreased regulatory T cells and increased levels of CD8+ T cells, activated NK cells, M1 macrophages, and M2 macrophages in colorectal cancer. However, there was no significant association between KMT2C/D LOF and TILs levels in other cancer types. Consistently, the results showed that KMT2C/D LOF variants were associated with prolonged overall survival only in colorectal cancer (p = 0.0485). We also presented that patients with KMT2C/D LOF mutations exhibited a better clinical response to anti-PD-1 therapy in a Chinese colorectal cancer cohort (p = 0.002). Taken together, these results suggested that KMT2C/D LOF variants could be a useful predictor for ICIs efficacy in colorectal cancer. In addition, the predictive value of KMT2C/D LOF variants was consistent with their association with TILs levels.

Promises and challenges of cardiac organoids.

Cardiovascular diseases are currently the main cause of death. The study of the pathogenesis and treatment of these diseases is still a major challenge. Traditional 2D cultured cells and animal models have certain limitations. Heart organoids as models can simulate the structure and function of the body, providing a new research strategy. This paper mainly discusses the development of organoids and their application in the study of the cardiac developmental process, drug screening and treatment of genetic and non-genetic diseases, concluding with their strengths and weaknesses.

Purification, characterization and inactivation kinetics of polyphenol oxidase extracted from Cistanche deserticola.

MAIN CONCLUSION: PPO was purified from Cistanche deserticola, and its enzymatic characteristics were clarified. It was found that microwave treatment was an efficient way to inactivate PPO. Polyphenol oxidase (PPO) from Cistanche deserticola was obtained and purified through an acetone precipitation and anion exchange column, the enzymatic characteristics and inactivation kinetics of PPO were studied. The specific activity of PPO was 73135.15 ± 6625.7 U/mg after purification, the purification multiple was 48.91 ± 4.43 times, and the recovery was 30.96 ± 0.27%. The molecular weight of the PPO component is about 66 kDa by SDS-PAGE analysis. The optimum substrate of PPO was catechol (Vmax = 0.048 U/mL, Km = 21.70 mM) and the optimum temperature and pH were 30 °C and 7, respectively. When the temperature is above 50 °C, pH < 3 or pH > 10, the enzyme activity can be significantly inhibited. The first-order kinetic fitting shows that microwave inactivation has lesser k values, larger D values and shorter t1/2. It was found that microwave treatment is considered as an efficient and feasible way to inactive PPO by comparing the Z values and Ea values of the two thermal treatments.

Exon skipping caused by splicing mutation in TNNT1 nemaline myopathy.

The TNNT1 gene encoding the slow skeletal muscle TnT has been identified as a causative gene for nemaline myopathy. TNNT1 nemaline myopathy is mainly characterized by neonatal-onset muscle weakness, pectus carinatum and respiratory insufficiency. Herein, we report on a Chinese girl with TNNT1 nemaline myopathy with mild clinical phenotypes without thoracic deformities or decreased respiratory function. Muscle biopsy showed moderate to marked type 1 fiber atrophy and nemaline rods. Next-generation sequencing identified the compound heterozygous c. 587dupA (p. D196Efs*41) and c. 387+5G>A mutations in the TNNT1 gene according to the transcript NM_003283.4. RNA sequencing revealed complete exon 9 skipping caused by the c. 387+5G>A mutation. Through quantitative PCR, we found that both the truncation c. 587dupA (p. D196Efs*41) and the splicing c. 387+5G>A mutations triggered nonsense-mediated mRNA decay (NMD). Western blotting showed the residual amount of the truncated TNNT1 protein by deletion of exon 9, which may ameliorate the disease to some extent.

Elevated high-sensitivity C-reactive protein levels increase the risk of new-onset cardiac conduction disorders.

BACKGROUND: Previous studies have reported that inflammatory responses can promote the onset of cardiovascular diseases; however, its association with cardiac conduction disorders remains unclear. The present community-based cohort study aimed to elucidate the effects of inflammatory responses on the risk of developing cardiac conduction disorders. METHODS: After the exclusion of participants failing to meet the inclusion criteria, 86,234 eligible participants (mean age: 50.57 ± 11.88 years) were included. The participants were divided into high-sensitivity C-reactive protein (hsCRP) ≤ 3 mg/L, and hsCRP > 3 mg/L groups based on hsCRP values. Multivariate Cox proportional hazard model was used to analyze the relationship between inflammatory responses and various cardiac conduction disorders. RESULTS: After adjusting for confounding factors, we observed that compared with the hsCRP ≤ 3 mg/L group, the hsCRP > 3 mg/L group exhibited increased risks of atrioventricular block (hazard ratio [HR]:1.64, 95%confidence interval [CI] 1.44-1.87) and left (HR:1.25, 95% CI 1.07-1.45) and right bundle branch block (HR:1.31, 95% CI 1.17-1.47). Moreover, the risk of various cardiac conduction disorders increased for every 1 standard deviation increase in log (hsCRP). The restricted cubic spline function confirmed a linear relationship between log (hsCRP) and the risk of developing cardiac conduction disorders (All nonlinearity P > 0.05). CONCLUSIONS: High hsCRP levels are an independent risk factor for cardiac conduction disorders, and hsCRP levels are dose-dependently associated with the risk of conduction disorders. Our study results may provide new strategies for preventing cardiac conduction disorders.

A simple strategy to obtain graphitic carbon nitride modified TiO2layer for efficient perovskite solar cells.

The power conversion efficiency (PCE) of perovskite solar cells (PSCs) can be improved through the concurrent strategies of enhancing charge transfer and passivating defects. Graphite carbon nitride (g-C3N4) has been demonstrated as a promising modifier for optimizing energy level alignment and reducing defect density in PSCs. However, its preparation process can be complicated. A simple one-step calcination approach was used in this study to prepare g-C3N4-modified TiO2via the incorporation of urea into the TiO2precursor. This modification simultaneously tunes the energy level alignment and passivates interface defects. The comprehensive research confirms that the addition of moderate amounts of g-C3N4to TiO2results in an ideal alignment of energy levels with perovskite, thereby enhancing the ability to separate and transfer charges. Additionally, the g-C3N4-modified perovskite films exhibit an increase in grain size and crystallinity, which reduces intrinsic defects density and extends charge recombination time. Therefore, the g-C3N4-modified PSC achieves a champion PCE of 20.00%, higher than that of the control PSC (17.15%). Our study provides a systematic comprehension of the interfacial engineering strategy and offers new insights into the development of high-performance PSCs.

Efficient identification of palatability-related genes using QTL mapping in rice breeding.

The gelatinization temperature of rice is an important factor in determining the eating and cooking quality, and it affects consumer preference. The alkali digestion value (ADV) is one of the main methods used to test the quality of rice and has a high correlation with the gelatinization temperature. For the development of high-quality rice, it is important to understand the genetic basis of palatability-related traits, and QTL analysis is a statistical method linking phenotypic data and genotype data and is an effective method to explain the genetic basis of variation in complex traits. QTL mapping related to the ADV of brown and milled rice was performed using the 120 Cheongcheong/Nagdong double haploid (CNDH) line. As a result, 12 QTLs related to ADV were detected, and 20 candidate genes were selected from the RM588-RM1163 region of chromosome 6 through screening by gene function analysis. The comparison of the relative expression level of candidate genes showed that OsSS1q6 is highly expressed in CNDH lines with high ADV in both brown rice and milled rice. In addition, OsSS1q6 has high homology with the starch synthase 1 protein and interacts with various starch biosynthesis-related proteins, such as GBSSII, SBE, and APL. Therefore, we suggest that OsSS1q6 identified through QTL mapping could be one of the various genes involved in the gelatinization temperature of rice by regulating starch biosynthesis. This study can be used as basic data for breeding high-quality rice and provides a new genetic resource that can increase the palatability of rice. Supplementary Information: The online version contains supplementary material available at 10.1007/s11032-023-01392-2.