A research team has uncovered the genetic mechanism behind hairlessness in wucai, a leafy vegetable widely grown in southern China. 

DNA methylation typically silences genes, but in citrus, a surprising reversal occurs.

Malaria remains one of the most devastating infectious diseases globally, with Plasmodium falciparum responsible for the majority of malaria-related deaths, particularly among children under five in sub-Saharan Africa. Despite decades of intensive control efforts and the widespread deployment of artemisinin-based combination therapies (ACTs), the emergence and spread of artemisinin resistance in Southeast Asia and its potential dissemination to Africa represent an urgent threat to global malaria control, underscoring the critical need for novel antimalarial drugs with innovative mechanisms of action. This perspective article explores a novel therapeutic strategy targeting the hemozoin detoxification pathway in Plasmodium falciparum, a process that is essential for parasite survival within infected erythrocytes and that has been validated as a drug target by the clinical success of chloroquine and other quinoline antimalarials. The authors propose that chlorophyll derivatives, specifically chlorin e6 and related compounds, could act as tetrapyrrole mimics that disrupt hemozoin formation by interfering with the biomineralization process through which the parasite detoxifies the toxic free heme released from hemoglobin digestion.

Nipah virus (NiV), a highly pathogenic zoonotic paramyxovirus, has emerged as a significant global public health threat due to its high mortality rate, potential for human-to-human transmission, and the absence of licensed vaccines or specific antiviral treatments. Since its initial identification in 1998 during an outbreak in Malaysia and Singapore, NiV has caused recurrent outbreaks in Bangladesh and India, with case fatality rates ranging from 40% to over 90%, and has been classified as a priority pathogen by the World Health Organization and the Coalition for Epidemic Preparedness Innovations. This perspective article provides a comprehensive international risk assessment of Nipah virus outbreaks and evaluates the medium- to long-term prevention and control prospects for China, a country that shares borders with endemic regions and possesses ecological conditions conducive to NiV transmission. The authors analyze the global epidemiology of NiV, including the natural reservoir (fruit bats of the Pteropus genus), transmission dynamics, and the factors driving outbreak emergence, such as deforestation, agricultural intensification, and increasing human-animal interface.

Gray mold can quietly follow blueberries from the field into storage, turning healthy-looking fruit into postharvest losses and narrowing the window for long-distance marketing. 

Congenital muscular dystrophies (CMDs) represent a genetically heterogeneous group of disorders characterized by muscle weakness, dystrophic changes on muscle biopsy, and onset typically in infancy or childhood. Variants in the INPP5K gene, which encodes a phosphoinositide 5-phosphatase that regulates phosphoinositide signaling, have recently been identified as a rare cause of congenital muscular dystrophy, commonly associated with early-onset cataracts and intellectual disability. This case report describes the first Chinese patient with INPP5K-related muscular dystrophy, a 28-year-old male with a notably mild phenotype that lacked intellectual disability, expanding the clinical spectrum of this disorder. The patient presented with bilateral cataracts requiring surgical correction at age 5, followed by adolescent-onset limb girdle weakness with postural hand tremors beginning at age 15 and progressive lower limb weakness at age 16. Muscle magnetic resonance imaging revealed a characteristic pattern of selective fatty infiltration, with severe involvement of gluteal and thigh muscles and striking sparing of the rectus femoris, sartorius, and gracilis muscles, a pattern that provides important diagnostic clues. Genetic analysis identified compound heterozygous novel INPP5K variants: a missense variant c.274C>T, p.(Arg92Cys), and a synonymous variant c.261G>A, p.(Lys87=).

Immune checkpoint inhibitor (ICI)-based immunotherapy has emerged as a transformative treatment strategy for stage III non-small cell lung cancer (NSCLC), significantly improving outcomes in both neoadjuvant and adjuvant settings. However, predictive biomarkers of response to immunotherapy remain limited, and identifying patients most likely to benefit from these treatments remains a critical unmet need. DNA polymerase epsilon (POLE) mutations, although rare in NSCLC, are associated with an increased tumor mutational burden (TMB) and enhanced neoantigen presentation, both of which are mechanistically linked to increased sensitivity to immune checkpoint inhibitor therapy. This case report describes a 52-year-old woman diagnosed with stage IIIA NSCLC whose tumor demonstrated negative programmed death-ligand 1 (PD-L1) expression, a factor typically associated with reduced likelihood of response to immunotherapy. Molecular profiling revealed a somatic POLE mutation (NM_006231.4: c.1270C>G, p.Leu424Val) in the absence of additional targetable tumor alterations. A perioperative chemo-immunotherapy approach was implemented, consisting of three cycles of neoadjuvant carboplatin, pemetrexed, and pembrolizumab, followed by curative-intent surgery. Restaging computed tomography after neoadjuvant therapy revealed a significant radiographic response, and histopathological examination of the surgical specimen demonstrated a pathological complete response (pCR), with no viable tumor cells identified.

Pontocerebellar hypoplasia type 12 (PCH12) is an ultra-rare, perinatally lethal neurodegenerative disorder characterized by profound microcephaly, pontocerebellar hypoplasia, and arthrogryposis, with onset typically occurring during prenatal development. Previous reports have associated PCH12 with biallelic complete loss-of-function variants in the COASY gene, which encodes coenzyme A synthase, a critical enzyme in the coenzyme A biosynthetic pathway. These variants have been identified in 14 fetuses and newborns from eight unrelated families worldwide. In contrast, COASY partial loss-of-function variants have been linked to COASY protein-associated neurodegeneration (CoPAN), a subtype of neurodegeneration with brain iron accumulation (NBIA) characterized by later onset and more protracted clinical course. Emerging evidence suggests COASY-related disorders may represent a phenotypic continuum between the severe PCH12 spectrum and the milder CoPAN spectrum, determined by the degree of residual COASY enzymatic activity. In this case report, the authors used exome sequencing to identify a novel variant combination in the COASY gene in a patient presenting with clinical features consistent with PCH12: a previously reported missense variant (c.641C>T, p.Ala214Val) in compound heterozygosity with a previously unreported rare nonsense variant (c.1015C>T, p.Arg339*).

Thrombotic thrombocytopenic purpura (TTP) is a rare but life-threatening hematological emergency defined by severe deficiency of ADAMTS13, a metalloproteinase that cleaves ultra-large von Willebrand factor multimers. However, TTP-like syndromes without ADAMTS13 reduction can occur in the context of systemic infections such as human immunodeficiency virus (HIV), posing significant diagnostic and therapeutic challenges, particularly in high-risk and underdiagnosed populations. This case report describes a 45-year-old transgender woman who presented with abdominal and lumbar pain, severe anemia, and thrombocytopenia. Laboratory evaluation revealed schistocytes on peripheral blood smear, elevated lactate dehydrogenase, and indirect hyperbilirubinemia, prompting a high PLASMIC score and urgent initiation of plasma exchange for suspected primary TTP. However, subsequent investigations revealed preserved ADAMTS13 activity, effectively excluding immune-mediated TTP, and uncovered a previously undiagnosed advanced HIV infection with profound immunosuppression (CD4+ T-cell count of 33 cells/µL), accompanied by active Epstein-Barr virus (EBV) and human herpesvirus 8 (HHV-8) viremia. Further evaluation revealed disseminated AIDS-related Kaposi's sarcoma. Despite timely initiation of antiretroviral therapy and comprehensive supportive care, the patient experienced progressive clinical deterioration and died on day 69 of hospitalization.

Hereditary spherocytosis (HS) and thalassemia are among the most common inherited hemolytic anemias, yet their co-occurrence presents unique diagnostic challenges due to overlapping clinical manifestations. This case report describes a unique presentation of concurrent hematological disorders in a 2-year-old Chinese boy: hereditary spherocytosis caused by a novel gene mutation, together with α-globin gene triplication. The child presented with a history of longstanding hemolytic disease, with recurrent episodes of anemia, jaundice, and abdominal pain triggered by upper respiratory infections, accompanied by splenomegaly and cholecystolithiasis. Laboratory evaluation revealed increased osmotic fragility of red blood cells and elevated reticulocyte count, supporting a diagnosis of hemolytic anemia. Mutation analysis identified a de novo heterozygous mutation in the SPTB gene: c.149-1G>A, a novel splicing mutation not detected in either parent and not previously reported in the literature. This pathogenic variant is speculated to affect pre-mRNA splicing of β-spectrin, a critical component of the erythrocyte cytoskeleton. Concurrently, the child was found to carry α-globin gene triplication (αααanti4.2), a relatively rare numerical variation that may complicate the clinical presentation by altering hemoglobin synthesis.