Axial Higgs mode detected by quantum pathway interference in RTe3.

The observation of the Higgs boson solidified the standard model of particle physics. However, explanations of anomalies (for example, dark matter) rely on further symmetry breaking, calling for an undiscovered axial Higgs mode1. The Higgs mode was also seen in magnetic, superconducting and charge density wave (CDW) systems2,3. Uncovering the vector properties of a low-energy mode is challenging, and requires going beyond typical spectroscopic or scattering techniques. Here we discover an axial Higgs mode in the CDW system RTe3 using the interference of quantum pathways. In RTe3 (R = La, Gd), the electronic ordering couples bands of equal or different angular momenta4-6. As such, the Raman scattering tensor associated with the Higgs mode contains both symmetric and antisymmetric components, which are excited via two distinct but degenerate pathways. This leads to constructive or destructive interference of these pathways, depending on the choice of the incident and Raman-scattered light polarization. The qualitative behaviour of the Raman spectra is well captured by an appropriate tight-binding model, including an axial Higgs mode. Elucidation of the antisymmetric component is direct evidence that the Higgs mode contains an axial vector representation (that is, a pseudo-angular momentum) and hints that the CDW is unconventional. Thus, we provide a means for measuring quantum properties of collective modes without resorting to extreme experimental conditions.

Correlation analysis between the amniotic fluid contamination and clinical grading of neonatal hypoxic-ischemic encephalopathy and biomarkers of brain damage.

BACKGROUND: Amniotic fluid contamination (AFC) is a risk factor for neonatal hypoxic ischemic encephalopathy (HIE); however, the correlation between AFC level and the incidence and clinical grading of HIE, in addition to relevant biomarkers of brain damage, have not been assessed. METHODS: This single-center observational study included 75 neonates with moderate-to-severe HIE. The neonates with HIE were divided into four subgroups according to the AFC level: normal amniotic fluid with HIE group (NAF-HIE), I°AFC with HIE group (I°AFC-HIE), II°AFC with HIE group (II°AFC-HIE), and III°AFC with HIE group (III°AFC-HIE). The control groups consisted of 35 healthy neonates. The clinical grading of neonatal HIE was performed according to the criteria of Sarnat and Sarnat. Serum tau protein and S100B were detected by enzyme-linked immunosorbent assay kits. Correlations of serum tau protein and S100B were evaluated using the Pearson correlation analysis. RESULTS: (1) The incidence of neonatal HIE in the NAF-HIE group was 20 cases (26. 7%), I°AFC-HIE was 13 cases (17.3%), II°AFC-HIE was 10 cases (13.3%), and III°AFC-HIE was 32 cases (42. 7%). The incidence of moderate-to-severe HIE in the I°-III°AFC-HIE groups was 73.3% (55/75). (2) In 44 cases with severe HIE, 26 cases (59.1%) occurred in the III°AFC-HIE group, which had a significantly higher incidence of severe HIE than moderate HIE (p < 0.05). In NAF-HIE and I°AFC-HIE groups, the incidence of moderate HIE was 45.2% and 29.0%, respectively, which was higher than that of severe HIE (X2 = 9.2425, p < 0.05; X2 = 5.0472, p < 0.05, respectively). (3) Serum tau protein and S100B levels in the HIE groups were significantly higher than in the control group (all p < 0.05), and were significantly higher in the III°AFC-HIE group than in the NAF-HIE and I°AFC-HIE groups (all p < 0.05). (4) Serum tau protein and S100B levels in the severe HIE group were significantly higher in the moderate HIE group (all p < 0.05). (5) Serum tau protein and S100B levels were significantly positively correlated (r = 0.7703, p < 0.0001). CONCLUSION: Among children with severe HIE, the incidence of III°AFC was higher, and the levels of serum tau protein and S100B were increased. AFC level might be associated with HIE grading.

Three Novel Heterozygous Mutations of NPHS1 Gene Causing Infants with Congenital Nephrotic Syndrome: Two Chinese (Han) Cases.

BACKGROUND: Congenital nephrotic syndrome (CNS) of the Finnish type (CNF) is an autosomal recessively disorder. NPHS1 gene mutation is the main gene responsible for CNF. This study aimed to explore the clinical manifestations and the characteristics of genetic variation in Chinese patients with CNS. METHODS: A 15-minute-old boy and a 34-day-old girl with CNS were included. NPHS1 gene was detected by next-generation high-throughput sequencing. RESULTS: Patient 1 carried two novel heterozygous mutations of NPHS1 gene, one was c.204delG, p. (Leu69fs) in exon 2 of NPHS1 gene, a heterozygote frameshift mutation; the other was c.3558delT, p. (Gly1187fs) in exon 28, a heterozygote frameshift mutation. Patient 2 carried three heterozygous mutations of NPHS1, among them, c.1561-G>A. p.Asp521Asn in exon 12 is a heterozygous missense mutation. It was identified as possible de novo pathogenicity gene. CONCLUSIONS: Three novel heterozygous mutations of NPHS1 gene were responsible for the patients with CNS and can enlarge the spectrum of NPHS1 gene mutation.

Colossal 3D Electrical Anisotropy of MoAlB Single Crystal.

3D anisotropic functional properties (such as magnetic, electrical, thermal, and optical properties, etc.) in a single material are not only beneficial to the multipurpose of a material, but also helpful to enrich the regulatory dimensionality of functional materials. Herein, a colossal 3D electrical anisotropy of layered MAB-phase MoAlB single crystal is introduced and dissected. Using high-temperature metal-solution method, high-quality MoAlB single crystals are obtained and a surprisingly strong out-of-plane (σa /σb  = 1.43 × 105 , at 2 K) and in-plane (σa /σc  = 12.12, at 2 K) electrical anisotropies are first observed. After a series of experimental and theoretical investigations, it is demonstrated that the 3D anisotropic crystal structure and chemical bond of MoAlB result in its 3D anisotropic phonon vibration and electronic structure, influence the corresponding electron-electron as well as electron-phonon interactions, and finally give rise to its colossal 3D anisotropy of electrical conductivity. This work experimentally and theoretically proves MoAlB single crystal possessing the 3D anisotropies of crystal structure, chemical bond, phonon vibration, electronic structure, and electrical transport, but also provides a promising platform for the future design of functionalized electronic devices as well as synthesis of new and large-sized in-plane anisotropic 2D material (MoBene).

Effect of Hypothermia on Serum Myelin Basic Protein and Tumor Necrosis Factor-α in Neonatal Hypoxic-Ischemic Encephalopathy.

OBJECTIVE: Multiple randomized controlled trials have shown that hypothermia is a safe and effective treatment for neonatal moderate or severe hypoxic-ischemic encephalopathy (HIE). The neuroprotective mechanisms of hypothermia need further study. The aim of this study was to investigate the effect of hypothermia on the serum levels of myelin basic protein (MBP) and tumor necrosis factor-α (TNF-α) as well as neurodevelopmental outcomes in neonatal HIE. STUDY DESIGN: Eighty-five neonates with moderate-to-severe HIE were divided into a hypothermia group (n = 49) and a control group (n = 36). Serum levels of MBP and TNF-α within 6 hours after birth and after 3 days of treatment were determined by enzyme-linked immunosorbent assay, and neurodevelopmental outcome at the age of 12 to 15 months was assessed by using the Gesell development scale. RESULTS: After 3 days of treatment, serum levels of MBP and TNF-α in the control group were not significantly different from levels before treatment (p > 0.05), and serum levels of MBP and TNF-α in the hypothermia group were significantly lower than levels before treatment (p < 0.05). Serum levels of MBP and TNF-α were significantly negatively correlated with developmental quotient (DQ; r = - 0.7945, p = 0.0000; r = - 0.7035, p = 0.0000, respectively). Serum levels of MBP and TNF-α in neurodevelopmentally impaired infants were significantly higher than those in infants with suspected neurodevelopmental impairment and those in neurodevelopmentally normal infants (both p < 0.01). The rate of reduction of neurodevelopmental impairment was higher among infants in the hypothermia group than among those in the control group (χ2 = 16.3900, p < 0.05). CONCLUSION: Hypothermia can reduce serum levels of MBP and TNF-α in neonates with HIE. Inhibiting the release of TNF-α may be one of the mechanisms by which hypothermia protects the myelin sheath. KEY POINTS: · Hypothermia can reduce serum levels of MBP and TNF-α in neonatal HIE.. · Hypothermia improves neurodevelopmental outcomes and reduces the rate of neurodevelopmental impairment.. · Hypothermia is a feasible and effective treatment for neonates with moderate or severe HIE..

Magnetism and Its Structural Coupling Effects in 2D Ising Ferromagnetic Insulator VI3.

van der Waals (vdW) magnets have emerged as a tunable platform for exploring a variety of layer-dependent magnetic phenomena. Here we probe the thickness-dependent magnetism of vanadium triiodide (VI3), a material known as a layered ferromagnetic Mott insulator in its bulk form, using magnetic circular dichroism microscopy. Robust ferromagnetism is observed in all thin layers, down to the monolayer limit with large coercive fields. In contrast to known vdW magnets, the Curie temperature shows an anomalous increase as the layer number decreases, reaching a maximum of 60 K in monolayers. Second harmonic generation measurements reveal broken inversion symmetry in exfoliated flakes, down to trilayers. This observation demonstrates that the exfoliated flakes take a layer stacking arrangement that differed from the inversion-symmetric parent bulk counterpart. Our results suggest a coupling effect between magnetic and structural degrees of freedom in VI3 and its potential for engineering layer and twist angle-dependent magnetic phenomena.

Stacking Domain Wall Magnons in Twisted van der Waals Magnets.

Using bilayer CrI_{3} as an example, we demonstrate that stacking domain walls in van der Waals magnets can host one-dimensional (1D) magnon channels, which have lower energies than bulk magnons. Interestingly, some magnon channels are hidden in magnetically homogeneous background and can only be inferred with the knowledge of stacking domain walls. Compared to 1D magnons confined in magnetic domain walls, 1D magnons in stacking domain walls are more stable against external perturbations. We show that the relaxed moiré superlattices of small-angle twisted bilayer CrI_{3} is a natural realization of stacking domain walls and host interconnected moiré magnon network. Our Letter reveals the importance of stacking domain walls in understanding magnetic properties of van der Waals magnets and extends the scope of stacking engineering to magnetic dynamics.

Neonate with Congenital Thrombotic Thrombocytopenic Purpura: a Case Report of a de novo Compound Heterozygote Mutation in ADAMTS13 Gene and Review of Literature.

BACKGROUND: Congenital thrombotic thrombocytopenic purpura (TTP) is rare and is prone to misdiagnosis or missed diagnosis in clinical. The relationship between genotype and phenotype needs further study. METHODS: A 15-hour-old Chinese girl develops jaundice. Her platelet counts suddenly decreases with bleeding spots on the left side of chest, upper abdomen, and bilateral groin on the fourth day after birth. The plasma ADAMTS13 activity and inhibitor are detected by residual collagen binding assay. ADAMTS 13 gene is detected by next generation sequencing. RESULTS: The plasma ADAMTS13 activity of the patient is shown to be severely deficient, but without inhibitor. Gene sequencing analysis shows that the patient carries a compound heterozygote mutation of ADAMTS13 gene, one is c.1564T>C, p.(Cys522Arg) on exon 13 of the ADAMTS13 gene, a heterozygote missense mutation. It is identified as a de novo suspected pathological variation. The other is c.330+1G>A on intron 3 of the ADAMTS13 gene, a heterozygote splicing mutation. Her father and elder sister carry c.1564T>C, p.(Cys522Arg) on exon 13 of the ADAMTS13 gene, a heterozygote missense mutations. Her mother carries c.330+1G>A on intron 3 of the ADAMTS13 gene, a heterozygote splicing mutation. CONCLUSIONS: The deficiency of ADAMTS13 caused by one heterozygote missense mutation and the other heterozygote splicing mutation are responsible for the episode of this congenital TTP patient.

Strong Electron-Phonon Coupling in the Excitonic Insulator Ta2NiSe5.

An excitonic insulating (EI) state is a fantastic correlated electron phase in condensed matter physics, driven by screened electron-hole interaction. Ta2NiSe5 is an excitonic insulator with a critical temperature (TC) of 328 K. In the current study, temperature-dependent Raman spectroscopy is used to investigate the phonon vibrations in Ta2NiSe5. The following observations were made: (1) an abnormal blue shift around TC is observed, which originates from the monoclinic to orthorhombic structural phase transition; (2) the splitting of a mode and two new Raman modes at 147 and 235 cm-1 have been observed with the formation of an EI state. With the help of first-principles calculations and temperature-dependent X-ray diffraction (XRD) experiments, it is found that the TaSe6 octahedra are "frozen" and the NiSe4 tetrahedra are greatly distorted below TC. Thus, it seems that the distortion of NiSe4 tetrahedra plays an important role in the strong electron-phonon coupling (EPC) in Ta2NiSe5, while the strong EPC, coupled with electron-hole interaction, opens the energy gap to form the EI state in Ta2NiSe5.

A Case Report of Primary Neonatal Hypocholinesterase Caused by Homozygous Frameshift Mutation of the utyrylcholinesterase (BCHE) Gene and Review of Literature.

BACKGROUND: Primary neonatal hypocholinesterase is rare; its genetic pattern and mutation still need to be further studied. METHODS: The patient and his parents are studied using next-generation sequencing technology. RESULTS: A boy one day after birth is admitted to the Neonatal Intensive Care Unit at our hospital after experiencing intermittent vomiting for 12 hours. The patient's serum cholinesterase level (113 - 283 U/L) is lower than normal value (4,000 - 12,600 U/L). Many factors of low serum cholinesterase are excluded. We highly suspect that it may be related to congenital factors. Molecular genetic test results show that the patient carried the BCHE gene (NM_000055.2) and has homozygous frameshift mutations at exon 2 c.401dupA (p.Asn134fs) of chromosome 3q26. It is a pathogenicity mutation. This locus mutation belongs to a novel pathogenic mutation. As a result of this mutation, the 134th amino acid Asn began to frameshift and the translation is terminated early. It can cause the Encoding of protein to truncate and lose its normal function. His parents' serum cholinesterase levels (father: 5,135 U/L; mother: 4,367 U/L) are in the normal value range, but his parents carried a heterozygous BCHE gene. CONCLUSIONS: This study suggests that gene sequence detection should be carried out early in hypocholinesterase of nknown cause in neonates. This study can not only improve understanding of the etiology and pathological mechanism of hypocholinesterase, but also it can enlarge the hypocholinesterase gene mutation spectrum.

Neonatal Crohn's disease with Oral ulcer as the first symptom caused by a compound heterozygote mutation in IL-10RA: a case report.

OBJECTIVE: To investigate the clinical and genetic characteristics of neonatal Crohn's disease (CD), improve recognition of neonatal CD, and reduce the number of patients that are missed or misdiagnosed. METHODS: A 10-day-old Chinese girl with oral ulcers was admitted to the Department of Neonatology. She later developed a rash and perianal disease, but without diarrhea and stool abnormalities. The patient and her parents underwent next-generation sequencing. RESULTS: The results showed that the patient carries a compound heterozygous mutation in the interleukin-10 receptor A (IL-10RA) (NM_001558.3) gene. One heterozygous mutation was c.301 c > T, P. (Arg 101 Trp) in exon 3 of IL-10RA (a missense mutation), and the other was c. 537G > A, P. (Thr 179 =) in exon 4 of IL 10RA (a synonymous mutation). The patient's father also carries the c.301 c > T, P. (Arg 101 Trp) heterozygous mutation in exon 3 of IL-10RA, whereas her mother carries the c.537G > A, P. (Thr 179 =) heterozygous mutation in exon 4 of IL-10RA. CONCLUSIONS: The results show that a compound heterozygous mutation in IL-10RA is associated with neonatal CD. Oral ulcers with a rash and perianal disease may be an early symptom of neonatal CD; therefore, such patients should undergo genetic identification as soon as possible.

SATB2-Associated Syndrome: a Case Report of a De Novo Nonsense Mutation in SATB2 from China and Review of Literature.

BACKGROUND: To study the clinical and genetic features from a Chinese child with SATB2-associated syndrome (SAS) and review of literature. METHODS: The girl, 2 years 3 months old, is admitted to the Department of Pediatric Rehabilitation in our hospital. This patient has mental retardation, language development disorder, cleft palate II0, micrognathia, malocclusion, irritability and bilateral oblique palpebral fissure as a clinical manifestation and is treated for 3 months. RESULTS: Gesell Development Scale (GDS) evaluation displays the patient's action capacity: gross motor 13.4, DQ 41%; fine motor 14.1, DQ 44%; adaptive behavior: DA 15.2, DQ 47%; speech capacity: DA 8.8; DQ 27%; person capacity: DA 11.7, DQ, 36%. Bayley Scale evaluation displays MDI < 50 and PDI < 50. Sleep EEG showed bilateral frontal pole - frontal - central - anterior temporal area presents in sharp wave, sharp and slow wave synchronization issue. A brain MRI showed that signal T2 is strengthened in the internal capsule hind leg. Flake T2FLATR high signal can been showed in the periventricular area of the parietal lobe in bilateral hemisphere. Molecular studies showed the patient carries a de novo nonsense mutation c.1285G>A (p.R429X) in SATB2. CONCLUSIONS: SATB2 mutation is not detected in the parents of the subjects. This study is important to further study the clinical features of SATB2-associated syndrome and to enlarge the SATB2 mutation spectrum.

Predictive Value of Neurodevelopmental Outcome and Serum Tau Protein Level in Neonates with Hypoxic Ischemic Encephalopathy.

BACKGROUND: Tau protein is s specific protein expressed by neurons in the central nervous system. Elevated serum Tau protein is associated with many diseases of the central nervous system. The serum Tau protein level in neonates with hypoxic ischemic encephalopathy (HIE) is still poorly understood. METHODS: Forty-one human neonates with HIE and thirty-five healthy neonates (control group) within 24 hours after birth were studied. Tau protein in serum was detected by enzyme-linked immunosorbent assay. Neurological outcome was assessed at 9 months of age according to the Gesell developmental scale. RESULTS: Tau protein in serum was significantly higher in the HIE group than in the control group (p < 0.01), in neonates with severe HIE than neonates with moderate HIE (p < 0.01), and in infants with neurodevelopmental retardation compared with those with normal neurodevelopment (p < 0.01). The result of this study showed an obvious negative correlation between the serum Tau protein level and development quotients of neonates with HIE (rs = -0.6172, p < 0.01). Receiver operator characteristic curve analysis showed that Tau protein (cutoff value 933.04 pg/mL) was a predictor of neurodevelopmental retardation outcome (AUC value = 0.860 (95% CI: 0.736 - 0.983, p < 0.01), sensitivity 100%, specificity 70.8%). CONCLUSIONS: Serum Tau protein level within 24 hours after birth can be used as a marker for the early diagnosis of neonatal HIE and predicting neurodevelopmental outcomes.

Protective effects of a green tea polyphenol, epigallocatechin-3-gallate, against sevoflurane-induced neuronal apoptosis involve regulation of CREB/BDNF/TrkB and PI3K/Akt/mTOR signalling pathways in neonatal mice.

Epigallocatechin-3-gallate (EGCG), a polyphenol in green tea, is an effective antioxidant and possesses neuroprotective effects. Brain-derived neurotrophic factor (BDNF) and cyclic AMP response element-binding protein (CREB) are crucial for neurogenesis and synaptic plasticity. In this study, we aimed to assess the protective effects of EGCG against sevoflurane-induced neurotoxicity in neonatal mice. Distinct groups of C57BL/6 mice were given EGCG (25, 50, or 75 mg/kg body weight) from postnatal day 3 (P3) to P21 and were subjected to sevoflurane (3%; 6 h) exposure on P7. EGCG significantly inhibited sevoflurane-induced neuroapoptosis as determined by Fluoro-Jade B staining and terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL). Increased levels of cleaved caspase-3, downregulated Bad and Bax, and significantly enhanced Bcl-2, Bcl-xL, xIAP, c-IAP-1, and survivin expression were observed. EGCG induced activation of the PI3K/Akt pathway as evidenced by increased Akt, phospho-Akt, GSK-3ß, phospho-GSK-3ß, and mTORc1 levels. Sevoflurane-mediated downregulation of cAMP/CREB and BDNF/TrkB signalling was inhibited by EGCG. Reverse transcription PCR analysis revealed enhanced BDNF and TrkB mRNA levels upon EGCG administration. Improved performance of mice in Morris water maze tests suggested enhanced learning and memory. The study indicates that EGCG was able to effectively inhibit sevoflurane-induced neurodegeneration and improve learning and memory retention of mice via activation of CREB/BDNF/TrkB-PI3K/Akt signalling.

Neonatal mortality and morbidity among infants between 24 to 31 complete weeks: a multicenter survey in China from 2013 to 2014.

BACKGROUND: The outcome of preterm infants has been varied in different hospitals and regions in developing countries. Regular clinical monitor are needed to know the effects of health care. This study aimed to describe the survival and morbidity rates of extreme to very preterm infants in 15 neonatal-intensive care hospitals in China. METHODS: Data were collected from January 1, 2013 to December 31, 2014 for preterm neonates with gestational age (GA) between 24 and 31 complete weeks born in hospitals from our collaborative study group. The primary outcomes were survival and major morbidities prior to hospital discharge. Major morbidities included bronchopulmonary dysplasia (BPD), intraventricular hemorrhage (IVH), necrotizing enterocolitis (NEC), retinopathy of prematurity (ROP), patent ductus arteriosus (PDA) and sepsis. Mutivariate logistic regression was used to analyze the risk factor influencing on the outcomes. RESULTS: The preterm birth rate was 9.9 % (13 701/138 240). The proportion of extreme to very preterm infants was 1.1 % and 11.8 % respectively. The survival rate prior to discharge was increased with increasing GA (0, 24 weeks; 28 %, 25 weeks; 84.8 %, 26 weeks; 83.5 %, 27 weeks; 87.4 %, 28 weeks; 90.7 %, 29 weeks; 93.9 %, 30 weeks; 96 %, 31 weeks). Rate of survival and without severe morbidity according to GA were 0 at 24 weeks, 8 % at 25 weeks, 60.6 % at 26 weeks; 53.2 % at 27 weeks; 62.3 % at 28 weeks; 67.9 % at 29 weeks; 79.1 % at 30 weeks, 85.8 % at 31 weeks respectively. Rate of antenatal steroid use was 56 %. The antenatal steroid use was lower in GA < 28 weeks infants than that in GA between 28 and 32 weeks (28-44.3 % vs 49.7-60.1 %, P < 0.05). Infants at the lowest GAs had a highest incidence of morbidities. Overall, 58.5 % had respiratory distress syndrome, 12.5 % bronchopulmonary dysplasia, 3.9 % necrotizing enterocolitis, 15.4 % intraventricular hemorrhage, 5.4 % retinopathy of prematurity, 28.4 % patent ductus arteriosus, and 9.7 % sepsis. Mortality and morbidity were influenced by gestational age (OR = 0.891, 95 % CI: 0.796-0.999, p = 0.0047 and OR = 0.666, 95 % CI: 0.645-0.688, p = 0.000 respectively), birth weight (OR = 0.520, 95 % CI: 0.420-0.643, p = 0.000 and OR = 0.921, 95 % CI: 0.851-0.997, p = 0.041 respectively), SGA (OR = 1.861, 95 % CI: 1.148-3.017, p = 0.012 and OR = 1.511, 95 % CI: 1.300-1.755, p = 0.000 respectively), Apgar score <7 at 5 min (OR = 1.947, 95 % CI: 1.269-2.987, p = 0.002 and OR = 2.262, 95 % CI: 1.950-2.624, p = 0.000 respectively). The survival rate was increased with more prenatal steroid use (OR = 1.615, 95 % CI: 1.233-1.901, p = 0.033). CONCLUSION: Although most of the preterm infants with GAs ≥26 weeks survived, a high complication in survivors still can be observed. Rate of survival of GAs less than 26 weeks was still low, and quality improvement methods should be used to look into increasing the use of antenatal steroids in the very preterm births.

[Expression of nesfatin-1/NUCB2 and ghrelin in gastric mucosa of rats with intrauterine growth retardation].

OBJECTIVE: To investigate the expression of nesfatin-1/NUCB2 and ghrelin in the gastric mucosa of rats with intrauterine growth retardation (IUGR) and its significance. METHODS: The IUGR animal model was established by feeding rats low-protein diets during their pregnancy. Newborn rats were divided into catch-up growth, non-catch-up growth and control groups. Protein and mRNA levels of nesfatin-1/NUCB2 and ghrelin in the gastric mucosa of rats were determined by RT-PCR and Western blot, respectively. RESULTS: Nesfatin-1/NUCB2 mRNA and protein were expressed in the gastric mucosa of rats immediately after birth, and their expression increased in an age-dependent manner in all three groups. Furthermore, the level of nesfatin-1/NUCB2 in the catch-up growth group was higher than that in the control group before weaning, whereas there was no significant difference in nesfatin-1/NUCB2 expression between the two groups after weaning. The level of nesfatin-1/NUCB2 in the non-catch-up growth group was lower than that in the catch-up growth group during the whole observation period. The level of ghrelin in the catch-up growth group was higher than that in the control group starting from day 12 after birth, whereas there was no significant difference in ghrelin expression between the two groups after weaning. The level of ghrelin in the non-catch-up growth group was lower compared with those in the catch-up growth and control groups from days 12 to 28 after birth. CONCLUSIONS: Nesfatin-1 and ghrelin are co-expressed in the gastric mucosa of rats with IUGR after birth and interact with each other to produce long-term nutritional regulation.

A biochemical feedback signal for hypothermia treatment for neonatal hypoxic-ischemic encephalopathy: focusing on central nervous system proteins in biofluids.

Hypothermia has been widely used to treat moderate to severe neonatal hypoxic-ischemic encephalopathy (HIE), yet evaluating the effects of hypothermia relies on clinical neurology, neuroimaging, amplitude-integrated electroencephalography, and follow-up data on patient outcomes. Biomarkers of brain injury have been considered for estimating the effects of hypothermia. Proteins specific to the central nervous system (CNS) are components of nervous tissue, and once the CNS is damaged, these proteins are released into biofluids (cerebrospinal fluid, blood, urine, tears, saliva), and they can be used as markers of brain damage. Clinical reports have shown that CNS-specific marker proteins (CNSPs) were early expressed in biofluids after brain damage and formed unique biochemical profiles. As a result, these markers may serve as an indicator for screening brain injury in infants, monitoring disease progression, identifying damage region of brain, and assessing the efficacy of neuroprotective measures. In clinical work, we have found that there are few reports on using CNSPs as biological signals in hypothermia for neonatal HIE. The aim of this article is to review the classification, origin, biochemical composition, and physiological function of CNSPs with changes in their expression levels after hypothermia for neonatal HIE. Hopefully, this review will improve the awareness of CNSPs among pediatricians, and encourage future studies exploring the mechanisms behind the effects of hypothermia on these CNSPs, in order to reduce the adverse outcome of neonatal HIE.

Fabrication of diosmin loaded food-grade bilayer nanoparticles with modified chitosan and soy peptides and antioxidant properties examination.

Diosmin is a flavonoid derived from plants, possessing anti-inflammatory, antioxidant, antidiabetic, neuroprotective and cardiovascular protective properties. However, diosmin has low solubility in water, leading to low bioavailability. In this study, we constructed bilayer nanoparticles with trimethyl chitosan and soy peptides to improve the oral bioaccessibility and bioavailability of diosmin, and determined the characteristics and antioxidant properties of the diosmin-loaded nanoparticles. The results showed that the size of the nanoparticles was around 250 nm with the encapsulation efficiency higher than 97 %, and the nanoparticles were stable under regular conditions. In vitro digestion suggested the nanoparticles could protect diosmin from releasing in gastric digestion but promote the bioaccessibility of diosmin in intestine. Furthermore, the diosmin-loaded nanoparticles presented excellent antioxidant activities in vitro and significantly decreased the Lipopolysaccharides-induced brain Malondialdehyde (MDA) level by oral administration. Therefore, the reported nanoparticles may be an effective platform for improving the oral bioavailability of diosmin.

Origin of the Anomalous Electrical Transport Behavior in Fe-Intercalated Weyl Semimetal Td -MoTe2.

Weyl semimetal Td -MoTe2 has recently attracted much attention due to its intriguing electronic properties and potential applications in spintronics. Here, Fe-intercalated Td -Fex MoTe2 single crystals (0 < x < 0.15 ) are grown successfully. The electrical and thermoelectric transport results consistently demonstrate that the phase transition temperature TS is gradually suppressed with increasing x. Theoretical calculation suggests that the increased energy of the Td phase, enhanced transition barrier, and more occupied bands in 1T' phase is responsible for the suppression in TS . In addition, a ρα -lnT behavior induced by Kondo effect is observed with x ≥ 0.08, due to the coupling between conduction carriers and the local magnetic moments of intercalated Fe atoms. For Td -Fe0.15 MoTe2 , a spin-glass transition occurs at ≈10 K. The calculated band structure of Td -Fe0.25 MoTe2 shows that two flat bands exist near the Fermi level, which are mainly contributed by the dyz and d x 2 - y 2 ${{\rm{d}}_{{x^2} - {y^2}}}$ orbitals of the Fe atoms. Finally, the electronic phase diagram of Td -Fex MoTe2 is established for the first time. This work provides a new route to control the structural instability and explore exotic electronic states for transition-metal dichalcogenides.

Polyphenolic Extracts of Coffee Cherry Husks Alleviated Colitis-Induced Neural Inflammation via NF-κB Signaling Regulation and Gut Microbiota Modification.

Coffee cherry husks, the main byproduct of coffee production, contain an abundance of polyphenols. In this study, dextran sodium sulfate (DSS)-induced colitis mice were used to study the protective effects of polyphenolic extracts of coffee cherry husks (CCHP) on inflammation. The results indicated that CCHP administration alleviated the histological changes of DSS-induced colitis in mice and downregulated the mRNA level of TNF-α, IL-1ß, IL-6 and Cox-2. Interestingly, CCHP inhibited the activation of microglia and suppressed neural inflammation in the brain. The TLR4/Myd88/NF-κB signaling pathway was examined and found to be inhibited by CCHP. Furthermore, a determination of the gut microbiota showed that an alteration of microbiota induced by DSS was restored by CCHP, including the decrease of the relative abundance of Proteobacteria and the increase of Bacteroidota. In conclusion, our results revealed the great potential of CCHP to alleviate brain inflammation in colitis mice by inhibiting the NF-κB signaling pathway and regulating gut microbiota.