Severe Coagulopathy and Intra-Alveolar Haemorrhage Due to Fat Malabsorption in Celiac Disease.

Celiac disease, a prevalent autoimmune disorder, can present atypically with fat malabsorption and coagulopathy due to vitamin K malabsorption. A 64-year-old male presented with haemoptysis and severe anaemia (Hb 6 g/dl). Despite normal previous coagulation tests, admission laboratory tests revealed an international normalised ratio (INR) of 7.0 and iron deficiency anaemia. Initial blood products and vitamin K treatment corrected the INR temporarily, but the patient's haemoptysis returned, and his INR values continued to rise. Further investigation revealed celiac disease with fat malabsorption, leading to vitamin K malabsorption and along with a previously prescribed antiplatelet aggregation therapy, this led to diffuse alveolar haemorrhage. A gluten-free diet and vitamin supplementation normalised the patient's INR and stopped the bleeding. This case highlights the importance of considering celiac disease in unexplained coagulopathies and the effectiveness of dietary management. LEARNING POINTS: Celiac disease can cause severe coagulopathy due to fat malabsorption and vitamin K deficiency.High suspicion is required for atypical presentations of celiac disease.A gluten-free diet is essential for managing celiac disease and normalising coagulation profiles.

Rapid diagnosis of coagulopathies from vitamin K deficiency in a consecutive case cohort evaluated by comparative assessment of factor II by 1-stage assays with prothrombin time vs Ecarin reagents.

BACKGROUND: Vitamin K (VK) deficiency (VKD) impairs γ-carboxylation of VK-dependent factors (VKDFs), resulting in higher factor (F)II levels measured by Ecarin (FIIE) reagents (that convert des-γ-carboxylated FII to meizothrombin) than by prothrombin time (FII) reagents. OBJECTIVES: To evaluate FII/FIIE abnormalities among patients assessed for coagulopathies and identify findings predictive of coagulopathy improvement after VK. METHODS: We retrospectively assessed consecutive cases from 2002 to 2021 with FII/FIIE tests and the sensitivity and specificity of FII/FIIE ratios and FIIE-FII differences for VKD defined as international normalized ratio correction/improvement of ≥0.5 after VK. RESULTS: Two hundred ninety-two patients (males, 58.2%; adults, 85.6%; median age, 73 years) were evaluated (84.2% hospitalized, 48.3% in intensive care, 71.6% with active liver disease, and 28% deceased at discharge) and 25% to 38% had FII/FIIE findings suggestive of VKD. Among 170 patients assessed for response to VK, FII/FIIE ratios of ≤0.84 to 0.91 and FIIE-FII differences of >0.04 U/mL had similar modest sensitivity (47.7%-69.3%) and modest to good specificity (67.1%-91.5%) for VKD. FII/FIIE ratios of <0.86, suggestive of VKD (sensitivity, 47.7%; specificity, 90.2%), were more common in patients deficient in only VKDF (P = .0001), but were detected in 16% with non-VKDF deficiencies. Low FIIE was commonly associated with active liver disease (P = .0002). Patients with and without probable VKD (based on FII/FIIE ratios of <0.86) had similar mortality, bleeding, and rates of prothrombin complex concentrate and red cell transfusions (P ≥ .78), but fewer with probable VKD received plasma and fibrinogen replacement (P ≤ .024). CONCLUSION: FII/FIIE comparison aids the diagnosis of VKD and predicts clinical responses to VK treatment among patients with coagulopathies.

A Case of Significant Coagulopathy Due to Vitamin K Deficiency Caused by the Administration of Cefazolin and Rifampicin and Hyponutrition After a Postoperative Infection of the Lumbar Spine.

Postoperative surgical site infection in the lumbar spine is one of the serious complications that sometimes results in death. Herein, we describe a case in which a patient was found to have coagulopathy due to vitamin K deficiency when he was transferred to a hospital for treatment for a postoperative infection of the lumbar spine. The coagulation disorder was caused by antimicrobial agents administered to the patient, who was suffering from hyponutrition. The patient was a 70-year-old man with a history of diabetes mellitus. He was diagnosed with lumbar spinal canal stenosis and underwent posterior decompression of the L2-L5 and S1 laminae at a previous hospital five months before transfer to our hospital. Four months before transfer, purulent discharge was observed from the wound, and methicillin-susceptible Staphylococcus aureus was detected in the wound culture. Cefazolin was administered for two weeks, resulting in initial improvement. However, one month before the transfer, the wound infection recurred, accompanied by bacteremia and a psoas abscess. He had been treated with cefazolin, levofloxacin, rifampicin, trimethoprim, and sulfamethoxazole, but the antibiotics' effects were insufficient. Upon transfer for debridement surgery due to uncontrolled infection, his coagulation parameters were as follows: prothrombin time (PT) 74.0 sec, PT-international normalized ratio (INR) 6.69, PT% 9.0, activated partial thromboplastin time (APTT) 138 sec, fibrinogen (FIB) 664 mg/dl, fibrin degradation products (FDP) 7.1 µg/ml, and protein induced by vitamin K absence-II (PIVKA-II) 34400 mAU/ml. Because we suspected vitamin K deficiency, vitamin K 40 mg was administered as a test dose, and coagulation function improved to PT 16.4 sec, PT-INR 1.30, PT% 65.2, and APTT 79 sec after four hours. The diagnosis of vitamin K deficiency was confirmed, vitamin K was administered for four days, and the coagulation status normalized five days after transfer. Debridement was performed for the left psoas abscess. Cefazolin was administered for eight weeks, and administration was completed. The coagulation abnormality did not recur due to careful attention to his nutrition. We experienced a case of coagulopathy due to vitamin K deficiency caused by antimicrobial agents administered to a hyponourished patient with a postoperative infection of the lumbar spine. The cause of vitamin K deficiency, in this case, was thought to be low nutrition, suppression of vitamin K-producing bacteria by cefazolin and rifampicin, and the use of cefazolin with a methyl-thiadiazole thiol group. It should be kept in mind that severe coagulopathy due to vitamin K deficiency caused by antimicrobial treatment with hyponutrition can occur in postoperative infections.

A Case of Vitamin K Deficiency Bleeding in a Newborn: Catastrophic Yet Preventable.

A four-week-old full-term male infant presented to the emergency department with blood in the diaper, increasing lethargy, and vomiting and was found to have multiple intracranial hemorrhages on CT. He was delivered at home and did not receive vitamin K. Coagulation studies were abnormal, and des-gamma carboxyprothrombin (DCP) was 481, diagnostic of vitamin K deficiency. He received vitamin K and required multiple antiepileptic medications for seizure control. Vitamin K deficiency bleeding (VKDB) is a preventable disease that can have devastating consequences and could present as early, classical, or late-onset. The typical presentation manifests with cutaneous, gastrointestinal, or intracranial hemorrhage most commonly in fully breastfed infants. Vitamin K prophylaxis has proven to be effective. With increasing out-of-hospital delivery and online misinformation, there is a declining administration of intramuscular vitamin K at birth. It is the responsibility of healthcare providers to properly inform patients and their families of the importance of vitamin K prophylaxis at or before the time of delivery.

Hemorrhagic Disease of the Newborn as a Consequence of Vitamin K Refusal Due to Language Barrier.

Newborns are prone to hemorrhagic disease due to vitamin K deficiency for multiple reasons, including vitamin K absence in breast milk and formula preparation, sterile gut with limited absorption, and lack of placental transfer. Despite the importance of vitamin K administration at birth in preventing hemorrhagic disease in infants, some parents still refuse administration to their newborns. One of the unexpected but preventable reasons is the language barrier related to special dialects, resulting in misunderstanding the benefits of vitamin K administration and complications related to vitamin K deficiency. We present a case of hemorrhagic disease of the newborn due to vitamin K deficiency following the parental refusal of postnatal prophylactic vitamin K due to a language barrier that resulted in miscommunication. Although appropriate education was provided to the family via Spanish interpreter as requested, it was later revealed that the family was speaking a special dialect, and they did not fully understand the importance of vitamin K prophylaxis. The patient experienced intracranial hemorrhage with full recovery after treatment and surgical intervention. Upon reviewing the case, the parents were speaking a rare dialect of Spanish, that was not known to the Spanish medical interpreters. A combination of a Spanish medical translator and a family friend was necessary for effective communication with the family.

Coagulopathy Induced by Antibiotics Usage and Bowel Obstruction With Colon Cancer: Report of a Rare Case.

This case report presents a rare occurrence of coagulopathy induced by antibiotics in a woman in her 90s with chronic bowel obstruction and massive colon cancer. The patient developed vitamin K deficiency-related coagulopathy following antibiotic administration, resulting in bleeding complications. Despite initial consideration of disseminated intravascular coagulation, further investigations revealed antibiotic-induced vitamin K deficiency. Prompt discontinuation of antibiotics and IV vitamin K2 administration led to the resolution of coagulopathy. The case emphasizes the importance of cautious antibiotic use in patients with chronic bowel obstruction and prolonged fasting. The protein induced by vitamin K absence-II (PIVKA-II) proved valuable in diagnosing vitamin K deficiency. The learning points include the potential for coagulopathy with antibiotics in prolonged bowel obstruction and the utility of PIVKA-II in assessing vitamin K deficiency. Healthcare providers should exercise caution when administering antibiotics in similar clinical scenarios.

Morpho-physiological, Genomic, and Transcriptional Diversities in Response to Potassium Deficiency in Rapeseed (Brassica napus L.) Genotypes.

Variations in the resistance to potassium (K) deficiency among rapeseed genotypes emphasize complicated regulatory mechanisms. In this study, a low-K-sensitivity accession (L49) responded to K deficiency with smaller biomasses, severe leaf chlorosis, weaker photosynthesis ability, and deformed stomata morphology compared to a low-K resistant accession (H280). H280 accumulated more K+ than L49 under low K. Whole-genome resequencing (WGS) revealed a total of 5,538,622 single nucleotide polymorphisms (SNPs) and 859,184 insertions/deletions (InDels) between H280 and L49. RNA-seq identified more differentially expressed K+ transporter genes with higher expression in H280 than in L49 under K deficiency. Based on the K+ profiles, differential expression profiling, weighted gene coexpression network analysis, and WGS data between H280 and L49, BnaC4.AKT1 was proposed to be mainly responsible for root K absorption-mediated low K resistance. BnaC4.AKT1 was expressed preferentially in the roots and localized on the plasma membrane. An SNP and an InDel found in the promoter region of BnaC4.AKT1 were proposed to be responsible for its differential expression between rapeseed genotypes. This study identified a gene resource for improving low-K resistance. It also facilitates an integrated knowledge of the differential physiological and transcriptional responses to K deficiency in rapeseed genotypes.

Severe Early-Onset Vitamin K Deficiency Bleeding in a Neonate Born to a Mother with Crohn's Disease in Clinical Remission: A Case Report.

Vitamin K deficiency bleeding (VKDB) in neonates is a significant disorder that causes skin, gastrointestinal, and intracranial hemorrhaging. Early-onset VKDB occurs within 24 hours of birth, and its prognosis is poor due to severe hemorrhage. The causes of early-onset VKDB include maternal intake of warfarin and anticoagulants, and maternal vitamin K deficiency. We report the case of a neonate with early-onset VKDB born to a mother with Crohn's disease. The neonate developed severe cerebellar hemorrhage on the day of birth and subsequent noncommunicating hydrocephalus requiring a ventriculoperitoneal shunt. The mother had a 14-year history of Crohn's disease and short bowel owing to intestinal resection. She was in complete remission during pregnancy according to the Crohn's Disease Activity Index. Endoscopic examination performed shortly before pregnancy revealed inflammatory findings in the residual small intestine. Her blood tests at delivery showed an elevated prothrombin induced by vitamin K deficiency or antagonist II (PIVKA-II) level of 26,900 mAU/mL. A definitive protocol to prevent early-onset VKDB in mothers with Crohn's disease complicated by a short bowel is lacking. Administering vitamin K to mothers with elevated PIVKA-II levels before delivery may help prevent early-onset VKDB.

Arabidopsis transcriptomic analysis reveals cesium inhibition of root growth involves abscisic acid signaling.

MAIN CONCLUSION: This is the first report on the involvement of abscisic acid signaling in regulating post-germination growth under Cs stress, not related to potassium deficiency. Cesium (Cs) is known to exert toxicity in plants by competition and interference with the transport of potassium (K). However, the precise mechanism of how Cs mediates its damaging effect is still unclear. This fact is mainly attributed to the large effects of lower K uptake in the presence of Cs that shadow other crucial effects by Cs that were not related to K. RNA-seq was conducted on Arabidopsis roots grown to identify putative genes that are functionally involved to investigate the difference between Cs stress and low K stress. Our transcriptome data demonstrated Cs-regulated genes only partially overlap to low K-regulated genes. In addition, the divergent expression trend of High-affinity K+ Transporter (HAK5) from D4 to D7 growth stage suggested participation of other molecular events besides low K uptake under Cs stress. Potassium deficiency triggers expression level change of the extracellular matrix, transfer/carrier, cell adhesion, calcium-binding, and DNA metabolism genes. Under Cs stress, genes encoding translational proteins, chromatin regulatory proteins, membrane trafficking proteins and defense immunity proteins were found to be primarily regulated. Pathway enrichment and protein network analyses of transcriptome data exhibit that Cs availability are associated with alteration of abscisic acid (ABA) signaling, photosynthesis activities and nitrogen metabolism. The phenotype response of ABA signaling mutants supported the observation and revealed Cs inhibition of root growth involved in ABA signaling pathway. The rather contrary response of loss-of-function mutant of Late Embryogenesis Abundant 7 (LEA7) and Translocator Protein (TSPO) further suggested low K stress and Cs stress may activate different salt tolerance responses. Further investigation on the crosstalk between K transport, signaling, and salt stress-responsive signal transduction will provide a deeper understanding of the mechanisms and molecular regulation underlying Cs toxicity.

Comparative physiological and transcriptome analysis between potassium-deficiency tolerant and sensitive sweetpotato genotypes in response to potassium-deficiency stress.

BACKGROUND: Sweetpotato is a typical ''potassium (K+) favoring'' food crop, which root differentiation process needs a large supply of potassium fertilizer and determine the final root yield. To further understand the regulatory network of the response to low potassium stress, here we analyze physiological and biochemical characteristics, and investigated root transcriptional changes in two sweetpotato genotypes, namely, - K tolerant "Xu32" and - K susceptible"NZ1". RESULT: We found Xu32 had the higher capability of K+ absorption than NZ1 with better growth performance, higher net photosynthetic rate and higher chlorophyll contents under low potassium stress, and identified 889 differentially expressed genes (DEGs) in Xu32, 634 DEGs in NZ1, 256 common DEGs in both Xu32 and NZ1. The Gene Ontology (GO) term in molecular function enrichment analysis revealed that the DEGs under low K+ stress are predominately involved in catalytic activity, binding, transporter activity and antioxidant activity. Moreover, the more numbers of identified DEGs in Xu32 than that in NZ1 responded to K+-deficiency belong to the process of photosynthesis, carbohydrate metabolism, ion transport, hormone signaling, stress-related and antioxidant system may result in different ability to K+-deficiency tolerance. The unique genes in Xu32 may make a great contribution to enhance low K+ tolerance, and provide useful information for the molecular regulation mechanism of K+-deficiency tolerance in sweetpotato. CONCLUSIONS: The common and distinct expression pattern between the two sweetpotato genotypes illuminate a complex mechanism response to low potassium exist in sweetpotato. The study provides some candidate genes, which can be used in sweetpotato breeding program for improving low potassium stress tolerance.

Clinical outcome and neurological development of patients with biliary atresia associated with a bleeding tendency: a single institution experience.

PURPOSE: We compared the clinical features of patients with biliary atresia (BA) associated with a bleeding tendency (BT) at the time of the diagnosis with those of patients without a bleeding tendency (NBT). METHODS: The patients' background characteristics, age in days at the first visit, Kasai portoenterostomy (KPE), and postoperative course were retrospectively analyzed. RESULTS: Nine of the 93 BA patients (9.7%) showed a BT, including 7 with intracranial hemorrhaging (ICH), 1 with gastrointestinal bleeding, and 1 with a prothrombin time (PT) of 0%. The age at the first visit was 62 ± 12 days old for BT patients and 53 ± 27 days old for NBT patients (p = 0.4); the age at KPE was 77 ± 9 days old for BT patients and 65 ± 24 days old for NBT patients (p = 0.2); the time from the first visit to surgery was 13 ± 7 days for BT patients and 11 ± 10 days for NBT patients (p = 0.5); and the native liver survival rate was 56% for BT patients and 58% for NBT patients (p = 1), with no significant difference in any of the parameters. The neurological outcomes of survivors of ICH were favorable. CONCLUSIONS: Appropriate BT correction allowed early KPE even after ICH, resulting in native liver survival rates comparable to those of NBT patients without significant neurological complications.

Intrauterine fetal death due to fetal intracranial hemorrhage associated with maternal vitamin K deficiency: A case report.

Vitamin K deficiency can cause coagulopathy; therefore, supplementation is recommended to prevent intracranial hemorrhage in newborns. Some reports have shown that maternal vitamin K deficiency is associated with intracranial hemorrhage in the fetus. However, no clear guidelines exist for the diagnosis and treatment of maternal vitamin K deficiency to prevent fetal intracranial hemorrhage. We report a case of intrauterine fetal death due to intracranial hemorrhage associated with maternal vitamin K deficiency resulting from hyperemesis gravidarum. In this case, maternal protein induced by vitamin K absence II (PIVKA-II) was high at the time of intrauterine fetal death. Therefore, measuring maternal PIVKA-II levels in high-risk cases may help determine the timing of therapeutic interventions for vitamin K deficiency during pregnancy.

Higher levels of circulating desphospho-uncarboxylated matrix Gla protein over time are associated with worse survival: the prospective Maastricht Intensive Care COVID cohort.

BACKGROUND: Extra-hepatic vitamin K-status, measured by dephosphorylated uncarboxylated matrix Gla protein (dp-ucMGP), maintains vascular health, with high levels reflecting poor vitamin K status. The occurrence of extra-hepatic vitamin K deficiency throughout the disease of COVID-19 and possible associations with pulmonary embolism (PE), and mortality in intensive care unit (ICU) patients has not been studied. The aim of this study was to investigated the association between dp-ucMGP, at endotracheal intubation (ETI) and both ICU and six months mortality. Furthermore, we studied the associations between serially measured dp-ucMGP and both PE and mortality. METHODS: We included 112 ICU patients with confirmed COVID-19. Over the course of 4 weeks after ETI, dp-ucMGP was measured serially. All patients underwent computed tomography pulmonary angiography (CTPA) to rule out PE. Results were adjusted for patient characteristics, disease severity scores, inflammation, renal function, history of coumarin use, and coronary artery calcification (CAC) scores. RESULTS: Per 100 pmol/L dp-ucMGP, at ETI, the odds ratio (OR) was 1.056 (95% CI: 0.977 to 1.141, p = 0.172) for ICU mortality and 1.059 (95% CI: 0.976 to 1.059, p = 0.170) for six months mortality. After adjustments for age, gender, and APACHE II score, the mean difference in plasma dp-ucMGP over time of ICU admission was 167 pmol/L (95% CI: 4 to 332, p = 0.047). After additional adjustments for c-reactive protein, creatinine, and history of coumarin use, the difference was 199 pmol/L (95% CI: 50 to 346, p = 0.010). After additional adjustment for CAC score the difference was 213 pmol/L (95% CI: 3 to 422, p = 0.051) higher in ICU non-survivors compared to the ICU survivors. The regression slope, indicating changes over time, did not differ. Moreover, dp-ucMGP was not associated with PE. CONCLUSION: ICU mortality in COVID-19 patients was associated with higher dp-ucMGP levels over 4 weeks, independent of age, gender, and APACHE II score, and not explained by inflammation, renal function, history of coumarin use, and CAC score. No association with PE was observed. At ETI, higher levels of dp-ucMGP were associated with higher OR for both ICU and six month mortality in crude and adjusted modes, although not statistically significantly.

Plasticity of wheat seedling responses to K+ deficiency highlighted by integrated phenotyping of roots and root hairs over the whole root system.

The availability in the soil of potassium (K+), a poorly mobile macronutrient required in large quantities for plant growth, is generally suboptimal for crop production in the absence of fertilization, making improvement of the ability of crops to adapt to K+ deficiency stress a major issue. Increasing the uptake capacity of the root system is among the main strategies to achieve this goal. Here, we report an integrative approach to examine the effect of K+ deficiency on the development of young plant entire root system, including root hairs which are known to provide a significant contribution to the uptake of poorly mobile nutrients such as K+, in two genetically distant wheat varieties. A rhizobox-type methodology was developed to obtain highly-resolved images of root and root hairs, allowing to describe global root and root hair traits over the whole root system via image analysis procedures. The two wheat varieties responded differently to the K+ shortage: Escandia, a wheat ancestor, reduced shoot biomass in condition of K+ shortage and substantially increased the surface area of its root system, specifically by increasing the total root hair area. Oued Zenati, a landrace, conversely appeared unresponsive to the K+ shortage but was shown to constitutively express, independently of the external K+ availability, favorable traits to cope with reduced K+ availability, among which a high total root hair area. Thus, valuable information on root system adaptation to K+ deficiency was provided by global analyses including root hairs, which should also be relevant for other nutrient stresses.

Association Between Vitamin Deficiencies and Ophthalmological Conditions.

Vitamin deficiencies can have adverse effects on health, including on the visual system. The ocular manifestations of a vitamin deficiency are related to the underlying biochemical function of the particular nutrient. While vitamin deficiencies are not common in developed counties, they are still prevalent in parts of the developing world and in specific, vulnerable populations. Vitamin deficiencies can cause or contribute to many ophthalmological conditions and eye diseases may even be the first presenting finding of a vitamin deficiency. As such, it is important for ophthalmologists to be aware of the ocular manifestations of vitamin deficiencies, especially given that the complications can be severe and effectively treated if identified early. This review summarizes the literature on the main vitamins known to have characteristic ocular manifestations: vitamins A, B1, B2, B9, B12, C, D, E and K. The function, epidemiology, manifestations, workup, and management of each vitamin is discussed in detail.

The Sweet Potato K+ Transporter IbHAK11 Regulates K+ Deficiency and High Salinity Stress Tolerance by Maintaining Positive Ion Homeostasis.

The K+ transporter KT/HAK/KUP (K+ transporter/high-affinity K+/K+ uptake) family has a critical effect on K+ uptake and translocation in plants under different environmental conditions. However, the functional analysis of KT/HAK/KUP members in sweet potatoes is still limited. The present work reported the physiological activity of a new gene, IbHAK11, in the KT/HAK/KUP family in sweet potatoes. IbHAK11 expression increased significantly in the low K+-tolerant line compared with the low K+-sensitive line following treatment with low K+ concentrations. IbHAK11 upregulation promoted root growth in Arabidopsis under low K+ conditions. Under high saline stress, transgenic lines had superior growth and photosynthetic characteristics compared with the wild-type (WT). As for IbHAK11-overexpressing plants, activation of both the non-enzymatic and enzymatic reactive oxygen species (ROS) scavenging systems was observed. Therefore, IbHAK11-overexpressing plants had lower malondialdehyde (MDA) and ROS levels (including H2O2 and O2-) compared with WT under salt-induced stress. We also found that under both low K+ and high salinity conditions, overexpression of IbHAK11 enhanced K+ translocation from the root to the shoot and decreased Na+ absorption in Arabidopsis. Consequently, IbHAK11 positively regulated K+ deficiency and high salinity stresses by regulating K+ translocation and Na+ uptake, thus maintaining K+/Na+ homeostasis in plants.

The Legal Limits of Parental Autonomy: Do Parents Have the Right to Refuse Intramuscular Vitamin K for Their Newborn?

Description The American Academy of Pediatrics recommends that all newborns receive an intra-muscular (IM) dose of vitamin K within 6 hours of delivery for the prevention of vitamin K deficiency bleeding (VKDB). There has been an increase in the number of parents who have refused the IM vitamin K dose for their infant based on its possible link to leukemia, preservatives that may lead to adverse reactions, and wanting to avoid pain for the infant. When newborns do not receive IM vitamin K, the most serious feared potential complication is intracranial hemorrhage with potential neurologic sequela including seizures, developmental delay, and death. Recent studies support the contention that parents are making the choice to refuse IM vitamin K without sufficient knowledge of the potential consequences. Parental decisions typically align with the best interest of the child; however, when parental decisions veer from the child's best interest, the limit of parental autonomy is tested. The precedent set by previous cases in which parental autonomy was challenged suggests parents should not be able to refuse IM vitamin K because the therapy has nearly no burden and forgoing this therapy has the potential for substantial harm. It has been argued that as long as the degree of intrusion is modest (a single IM injection) and the benefit substantial (prevention of possible death), states are granted the power to mandate the use of such an intervention. Mandated IM vitamin K for all newborns, regardless of parental approval, would rescind some parental autonomy but improve overall beneficence, nonmaleficence, and justice in the care of newborns.

Rice potassium transporter OsHAK18 mediates phloem K+ loading and redistribution.

High-affinity K+ transporters/K+ uptake permeases/K+ transporters (HAK/KUP/KT) are important pathways mediating K+ transport across cell membranes, which function in maintaining K+ homeostasis during plant growth and stress response. An increasing number of studies have shown that HAK/KUP/KT transporters play crucial roles in root K+ uptake and root-to-shoot translocation. However, whether HAK/KUP/KT transporters also function in phloem K+ translocation remain unclear. In this study, we revealed that a phloem-localized rice HAK/KUP/KT transporter, OsHAK18, mediated cell K+ uptake when expressed in yeast, Escherichia coli and Arabidopsis. It was localized at the plasma membrane. Disruption of OsHAK18 rendered rice seedlings insensitive to low-K+ (LK) stress. After LK stress, some WT leaves showed severe wilting and chlorosis, whereas the corresponding leaves of oshak18 mutant lines (a Tos17 insertion line and two CRISPR lines) remained green and unwilted. Compared with WT, the oshak18 mutants accumulated more K+ in shoots but less K+ in roots after LK stress, leading to a higher shoot/root ratio of K+ per plant. Disruption of OsHAK18 does not affect root K+ uptake and K+ level in xylem sap, but it significantly decreases phloem K+ concentration and inhibits root-to-shoot-to-root K+ (Rb+ ) translocation in split-root assay. These results reveal that OsHAK18 mediates phloem K+ loading and redistribution, whose disruption is in favor of shoot K+ retention under LK stress. Our findings expand the understanding of HAK/KUP/KT transporters' functions and provide a promising strategy for improving rice tolerance to K+ deficiency.

Aspergillus aculeatus enhances nutrient uptake and forage quality in bermudagrass by increasing phosphorus and potassium availability.

Introduction: Potassium and phosphorus are essential macronutrients for plant growth and development. However, most P and K exist in insoluble forms, which are difficult for plants to directly absorb and utilize, thereby resulting in growth retardation of plants under P or K deficiency stress. The Aspergillus aculeatus fungus has growth-promoting characteristics and the ability to dissolve P and K. Methods: Here, to investigate the physiological effects of A. aculeatus on bermudagrass under P or K deficiency, A. aculeatus and bermudagrass were used as experimental materials. Results and discussion: The results showed that A. aculeatus could promote tolerance to P or K deficiency stress in bermudagrass, decrease the rate of leaf death, and increase the contents of crude fat as well as crude protein. In addition, A. aculeatus significantly enhanced the chlorophyll a+b and carotenoid contents. Moreover, under P or K deficiency stress, bermudagrass inoculated with A. aculeatus showed higher N, P, and K contents than non-inoculated plants. Furthermore, exogenous A. aculeatus markedly decreased the H2O2 level and CAT and POD activities. Based on our results, A. aculeatus could effectively improve the forage quality of bermudagrass and alleviate the negative effects of P or K deficiency stress, thereby playing a positive economic role in the forage industry.

Radial nerve palsy caused by a rapidly growing intramuscular hematoma in an infant with biliary atresia: a case report.

BACKGROUND: Biliary atresia (BA) is a rare cause of persistent jaundice in infants that can result in vitamin K malabsorption and vitamin K deficiency bleeding (VKDB). We present an infant with BA who developed a rapidly growing intramuscular hematoma in her upper arm after a vaccination which caused a radial nerve palsy. CASE PRESENTATION: An 82-day-old girl was referred to our hospital because of a rapidly growing left upper arm mass. She had received three doses of oral vitamin K before age 1 month. At age 66 days, she received a pneumococcal vaccination in her left upper arm. On presentation, she showed no left wrist or finger extension. Blood examination revealed direct hyperbilirubinemia, liver dysfunction, and coagulation abnormalities, indicating obstructive jaundice. Magnetic resonance imaging showed a hematoma in the left triceps brachii. Abdominal ultrasonography revealed an atrophic gallbladder and the triangular cord sign anterior to the portal vein bifurcation. BA was confirmed on cholangiography. VKDB resulting from BA in conjunction with vaccination in the left upper arm were considered the cause of the hematoma. The hematoma was considered the cause of her radial nerve palsy. Although she underwent Kasai hepatic portoenterostomy at age 82 days, the obstructive jaundice did not sufficiently improve. She then underwent living-related liver transplantation at age 8 months. The wrist drop was still present at age 1 year despite hematoma resolution. CONCLUSIONS: Delayed detection of BA and inadequate prevention of VKDB can result in permanent peripheral neuropathy.