Histomorphological analysis of perfusion parameters and CNS lymphatic vessels in mice: an experimental method study.

To investigate the distribution and characteristics of lymphatic vessels within the central nervous system, we focus on the meninges of the spinal cord and brain parenchyma in mice. Additionally, we aim to provide experimental methods for obtaining optimal imaging and clear structures of lymphatic vessels, while optimizing the perfusion parameters to improve histomorphological quality. Male C57BL/6J mice were randomly divided into four groups, with each group assigned a specific perfusion parameter based on perfusion volumes and temperatures. Immunofluorescence staining of lymphatics and blood vessels was performed on both meningeal and the brain tissue samples. Statistical analysis was performed using one-way analysis of variance to compare the groups, and a significant level of P < 0.05 was considered statistically significant. Our study reports the presence of lymphatic vessels in the meninges of the spinal cord and brain parenchyma in mice. We highlight the crucial role of high perfusion volume of paraformaldehyde with low temperature in fixation for achieving optimal results. We provide experimental methods for obtaining optimal imaging and clear structures of lymphatic vessels in the meninges of the spinal cord and brain parenchyma in mice, which contribute to our understanding of the distribution and characteristics of lymphatic vessels within the central nervous system. Further research is warranted to explore the functional implications of these lymphatic vessels and their potential therapeutic significance in neurodegenerative and neuroinflammatory diseases.

Blockade of adenosine A2A receptors reverses early spatial memory defects in the APP/PS1 mouse model of Alzheimer's disease by promoting synaptic plasticity of adult-born granule cells.

BACKGROUND: The over-activation of adenosine A2A receptors (A2AR) is closely implicated in cognitive impairments of Alzheimer's disease (AD). Growing evidence shows that A2AR blockade possesses neuroprotective effects on AD. Spatial navigation impairment is an early manifestation of cognitive deficits in AD. However, whether A2AR blockade can prevent early impairments in spatial cognitive function and the underlying mechanism is still unclear. METHODS: A transgenic APP/PS1 mouse model of AD amyloidosis was used in this study. Behavioral tests were conducted to observe the protective effects of A2AR blockade on early spatial memory deficits in 4-month old APP/PS1 mice. To investigate the underlying synaptic mechanism of the protective effects of A2AR blockade, we further examined long-term potentiation (LTP) and network excitation/inhibition balance of dentate gyrus (DG) region, which is relevant to unique synaptic functions of immature adult-born granule cells (abGCs). Subsequently, the protective effects of A2AR blockade on dendritic morphology and synaptic plasticity of 6-week-old abGCs was investigated using retrovirus infection and electrophysiological recordings. The molecular mechanisms underlying neuroprotective properties of A2AR blockade on the synaptic plasticity of abGCs were further explored using molecular biology methods. RESULTS: APP/PS1 mice displayed DG-dependent spatial memory deficits at an early stage. Additionally, impaired LTP and an imbalance in network excitation/inhibition were observed in the DG region of APP/PS1 mice, indicating synaptic structural and functional abnormalities of abGCs. A2AR was found to be upregulated in the hippocampus of the APP/PS1 mouse model of AD. Treatment with the selective A2AR antagonist SCH58261 for three weeks significantly ameliorated spatial memory deficits in APP/PS1 mice and markedly restored LTP and network excitation/inhibition balance in the DG region. Moreover, SCH58261 treatment restored dendritic morphology complexity and enhanced synaptic plasticity of abGCs in APP/PS1 mice. Furthermore, SCH58261 treatment alleviated the impairment of synaptic plasticity in abGCs. It achieved this by remodeling the subunit composition of NMDA receptors and increasing the proportion of NR2B receptors in abGCs of APP/PS1 mice. CONCLUSIONS: Blockade of A2AR improves early spatial memory deficits in APP/PS1 mice, possibly by reversing synaptic defects of abGCs. This finding suggests that A2AR blockade could be a potential therapy for AD.

Genetic and neural mechanisms of sleep disorders in children with autism spectrum disorder: a review.

Background: The incidence of sleep disorders in children with autism spectrum disorder (ASD) is very high. Sleep disorders can exacerbate the development of ASD and impose a heavy burden on families and society. The pathological mechanism of sleep disorders in autism is complex, but gene mutations and neural abnormalities may be involved. Methods: In this review, we examined literature addressing the genetic and neural mechanisms of sleep disorders in children with ASD. The databases PubMed and Scopus were searched for eligible studies published between 2013 and 2023. Results: Prolonged awakenings of children with ASD may be caused by the following processes. Mutations in the MECP2, VGAT and SLC6A1 genes can decrease GABA inhibition on neurons in the locus coeruleus, leading to hyperactivity of noradrenergic neurons and prolonged awakenings in children with ASD. Mutations in the HRH1, HRH2, and HRH3 genes heighten the expression of histamine receptors in the posterior hypothalamus, potentially intensifying histamine's ability to promote arousal. Mutations in the KCNQ3 and PCDH10 genes cause atypical modulation of amygdala impact on orexinergic neurons, potentially causing hyperexcitability of the hypothalamic orexin system. Mutations in the AHI1, ARHGEF10, UBE3A, and SLC6A3 genes affect dopamine synthesis, catabolism, and reuptake processes, which can elevate dopamine concentrations in the midbrain. Secondly, non-rapid eye movement sleep disorder is closely related to the lack of butyric acid, iron deficiency and dysfunction of the thalamic reticular nucleus induced by PTCHD1 gene alterations. Thirdly, mutations in the HTR2A, SLC6A4, MAOA, MAOB, TPH2, VMATs, SHANK3, and CADPS2 genes induce structural and functional abnormalities of the dorsal raphe nucleus (DRN) and amygdala, which may disturb REM sleep. In addition, the decrease in melatonin levels caused by ASMT, MTNR1A, and MTNR1B gene mutations, along with functional abnormalities of basal forebrain cholinergic neurons, may lead to abnormal sleep-wake rhythm transitions. Conclusion: Our review revealed that the functional and structural abnormalities of sleep-wake related neural circuits induced by gene mutations are strongly correlated with sleep disorders in children with ASD. Exploring the neural mechanisms of sleep disorders and the underlying genetic pathology in children with ASD is significant for further studies of therapy.

Combined Relativistic Ab Initio Multireference and Experimental Study of the Electronic Structure of Terbium Luminescent Compound.

A new terbium (III) luminescent compound {[Tb2(PDC)2(ox)(H2O)4](H2O)2}n was synthesized by the self-assembly of Tb3+ ions with 3,5-pyridinedicarboxylate (PDC) and oxalate (ox) ligands and characterized by fluorescence spectroscopy and single-crystal X-ray diffraction. The density functional theory (DFT) and high-level correlated ab initio wave function methods with Spin-Orbit Coupling correction (CASSCF/SO and CAS-NEVPT2/SOC) were successfully applied to predict the absorption and emission spectra of this strongly correlated lanthanide system in excellent agreement with the experimental results.

Two New Anthraquinones from the Roots of Prismatomeris connata.

Two new anthraquinones, 4-hydroxy-1,2,3-trimethoxy-7-hydroxymethylanthracene-9,10-dione (1) and 1,2,3-trimethoxy-7-hydroxymethylanthracene-9,10- dione (2), were isolated from the roots of Prismatomeris connata, a Chinese medicinal herb. Their structures were elucidated by spectroscopic analysis. Compound 1 exhibited cytotoxicity against a panel of H1229, HTB 179, A549 and H520 lung tumor cell lines with IC50 values ranging from 12.3 to 20 µM.

Bartonella Species Detected in the Plateau Pikas (Ochotona curzoiae) from Qinghai Plateau in China.

Bartonella species can infect a variety of mammalian hosts and cause a broad spectrum of diseases in humans, but there have been no reports of Bartonella infection in Ochotonidae. This is the first study to detect Bartonella in plateau pikas in the Qinghai plateau, providing baseline data for the risk assessment of human Bartonella infection in this area. We obtained 15 Bartonella strains from 79 pikas in Binggou and Maixiu areas of Qinghai with a positive rate of 18.99%. Based on the phylogenetic analysis of the Bartonella citrate synthase (gltA) gene sequences, most strains were closely related to B. taylorii (3/15) and B. grahamii (12/15). The latter is a pathogenic strain in humans. Our results suggest that a corresponding prevention and control strategy should be taken into consideration in the Qinghai province.

Crystal structure of catena-poly[[di-aqua(4,5-di-aza-fluoren-9-one-κ(2) N,N')cadmium]-µ-2-hydroxy-5-sulfonato-benzoato-κ(3) O (1),O (1'):O (5)].

In the polymeric title compound, [Cd(C7H4O6S)(C11H6N2O)(H2O)2] n , the Cd(2+) atom is seven-coordinated by two water O atoms, by three O atoms from two 2-hy-droxy-5-sulfonato-benzoate (Hssal(2-)) ligands and by two N atoms from a 4,5-di-aza-fluoren-9-one (Dafo) ligand in a distorted penta-gonal-bipyramidal geometry. The Cd(2+) atoms are monodentately coordinated by the sulfonate group of one Hssal(2-) ligand and bidentately coordinated by the carboxyl-ate group of another Hssal(2-) ligand, generating zigzag chains running parallel to [010]. The chains are linked by O-H⋯O hydrogen bonds into a three-dimensional architecture.

Classifications of clinical and bowel morphological changes and their relationship with characteristics of patients with incarcerated groin hernias.

BACKGROUND: There is currently no grading standard for the degree of clinical and bowel morphological changes. The objective of this study was to define clinical and bowel morphological classifications and investigate the possible relationship with the characteristics of patients with incarcerated groin hernias. MATERIAL AND METHODS: We retrospectively studied 195 patients who underwent emergency hernia repair with simultaneous bowel resection between January 1992 and January 2012. We classified the degree of clinical and bowel morphological changes into 3 grades based on the incarceration time, intestinal morphology after damage, hernia sac integrity, degree of inflammation, and the presence/absence of bacterial growth, peritonitis signs, mechanical obstruction, cellulitis, and systemic shock. We also recorded patient characteristics and analyzed their relationships with these degrees according to our grading system. RESULTS: We identified 134, 42, and 19 cases of Grades I, II, and III of clinical and bowel morphological changes, respectively. Pearson's chi-squared tests revealed that advanced age (P=0.001), presence of comorbid disease (P=0.002), and high American Society of Anesthesiologists (ASA) score (P=0.017) were related to the degree. Morbidity and mortality also showed significant relationships with the degree (P<0.001, P=0.005, respectively), especially with regard to post-operative infection. CONCLUSIONS: The proposed 3-stage classifications of clinical and bowel morphological changes can be used to objectively reflect the degree of bowel damage. Greater levels of the changes were associated with higher incidences of complications and increased mortality, especially for older patients with comorbid diseases and poor ASA scores. Urgent surgery should be performed to avoid bowel damage exacerbation.

Crystal structure of poly[µ6-adipato-di-aquadi-µ2-oxalato-didysprosium(III)].

In the title coordination polymer, [Dy2(C6H8O4)(C2O4)2(H2O)2] n , the asymmetric unit consists of one Dy(3+) cation, one half of an adipate anion, two halves of oxalate anions and one coordinating water mol-ecule. The adipate and oxalate ions are located on centres of inversion. The Dy(3+) cation has a distorted tricapped trigonal-prismatic geometry and is coordinated by nine O atoms, four belonging to three adipate anions, four to two oxalate anions and one from an aqua ligand. The cations are bridged by adipate ligands, generating a two-dimensional network parallel to (010). This network is further extended into three dimensions by coordination of the rigid oxalate ligands and is further consolidated by O-H⋯O hydrogen bonds. A part of the adipate anion is disordered over two positions in a 0.75:0.25 ratio.

Sensitive bioassay for detection of PPARα potentially hazardous ligands with gold nanoparticle probe.

There are so many kinds of peroxisome proliferator-activated receptor α (PPARα) ligands with hazardous effect for human health in the environment, such as certain herbicides, plasticizers and drugs. Among these agonists, perfluorooctane sulfonate (PFOS), perfluorooctanoic acid (PFOA), and mono-(2-ethylhexyl) phthalate (MEHP) are mostly investigated due to their persistence and accumulation in environment and their potential toxicity via PPARα. This investigation aims at developing a bioassay method to detect PPARα ligands based on the ligand-receptor interaction on microplate. PPARα, which formed heterodimers with retinoid X receptor-α (RXRα), were activated by PPARα ligands to form ligands-PPARα-RXRα complexes. Then the complexes were transferred into a microplate and captured via monoclonal anti-PPARα antibody. The PPARα responsive elements (PPRE) modified-gold nanoparticle probes were captured by the ligand-PPARα-RXRα complexes immobilized on the microplate, and then could be quantified through measuring the optical density after silver enhancement. The results showed that PFOS was quantified with a linear range from 100 pM to 1 µM and the detection limit was 10 pM. In addition to PFOS, PFOA and MEHP were also quantified within a proper range through the proposed bioassay. This bioassay was compared with that of liquid chromatography tandem-mass spectrometry (LC-MS) for water spiked samples with a significant correlation (r = 0.9893). This study provides a high-throughput detection method for PPARα ligands in microplate with high sensitivity and wide linear range. It may serve as an assistant of LC-MS for prescreening of PPARα ligands like PFOS.

Protective effect of C(60) -methionine derivate on lead-exposed human SH-SY5Y neuroblastoma cells.

Oxidative stress has been considered as one of the possible mechanisms leading to the neurotoxicity of lead. One of the effective ways to prevent cellular damage after lead exposure is using antioxidants. In this paper, a novel C(60) -methionine derivate (FMD), a fullerene molecule modified with methionine, was synthesized. The protective effect of FMD on lead-exposed human SH-SY5Y neuroblastoma cells was investigated. In this research, after incubating with 500 µm Pb acetate alone for 72 h, the cells had undergone a series of biological changes including viability loss, apoptotic death, the depletion of glutathione (GSH), the peroxidation of membrane lipid and DNA damage. Pretreatment with FMD before lead exposure could improve cell survival, increase the GSH level, reduce malondialdehyde content and attenuate DNA damage without obvious toxicity. In addition, the protective effects of FMD were proven to be greater than those of other two C(60) -amino acid derivates, ß-alanine C(60) derivate and cystine C(60) derivate, which have been confirmed in our previous work to be able to protect rat pheochromocytoma PC12 cells from hydrogen dioxide-induced oxidative injuries. These observations suggest that FMD may serve as a potential antioxidative and neuroprotective agent in the prevention of lead intoxication.

Poly[µ(6)-adipato-diaquadi-µ(2)-oxalato-digadolinium(III)].

In the centrosymmetric title compound, [Gd(2)(C(6)H(8)O(4))(C(2)O(4))(2)(H(2)O)(2)](n), the Gd(3+) cations are each coordinated by nine O atoms, three from adipate anions, two from oxalate anions and one from an aqua ligand, completing a distorted tricapped trigonal-prismatic geometry. These tricapped trigonal prisms are bridged by the adipate ligands, generating layers lying parallel to (010). The coordination polymer layers are linked into a three-dimensional framework by the rigid oxalate ligands. The adipate and oxalate ions are all located on centers of inversion. A part of the adipate anion is disordered over two positions in a 0.75:0.25 ratio.

Poly[diaqua-µ(2)-oxalato-di-µ(4)-terephthalato-diytterbium(III)].

The crystal structure of the title complex, [Yb(2)(C(8)H(4)O(4))(2)(C(2)O(4))(H(2)O)(2)](n), features an extended three-dimensional framework made up of Yb(3+) ions coordinated by terephthalate ligands, oxalate ligands and water mol-ecules. The Yb(3+) ion has a distorted square-anti-prismatic coordination formed by one aqua ligand, two O atoms from an oxalate ligand and five O atoms belonging to four terephthalate anions. Two symmetry-independent terephthalate anions, as well as the oxalate anion, occupy special positions on inversion centers. The water molecule participates in O-H⋯O hydrogen bonding with both terephthalate anions.

Poly[diaqua-µ(2)-oxalato-di-µ(4)-succinato-diyttrium(III)].

In the title compound, [Y(2)(C(4)H(4)O(4))(2)(C(2)O(4))(H(2)O)(2)](n), the flexible succinate anion assumes a gauche conformation and bridges the eight-coordinated Y atoms, generating two-dimensional layers parallel to (010). The coordination polymer layers are linked into a three-dimensional framework by the rigid oxalate ligands. The oxalate ions are located on a center of inversion. Inter-molecular O-H⋯O hydrogen bonds help to stabilize the crystal structure.

Poly[diaqua-µ(2)-oxalato-di-µ(4)-terephthalato-dilutetium(III)].

In the title compound, [Lu(2)(C(8)H(4)O(4))(2)(C(2)O(4))(H(2)O)(2)](n), the Lu(3+) cations are each coordinated by eight O atoms of four terephthalate anions, one oxalate anion and one aqua ligand to complete a distorted square-anti-prismatic geometry. They are bridged by the terephthalate ligands, generating a three-dimensional framework, which is further stabilized by the oxalate ligands. The terephthalate ions and oxalate ions are all located on centers of inversion.

Dermoid cyst of the posterior fossa associated with congenital dermal sinus in a child.

BACKGROUND: Intracranial dermoid cysts are congenital benign neoplasms. Hydrocephalus and abscess as the principal manifestations of the posterior fossa dermoid cyst are rare. We present a case of obstructive hydrocephalus and abscess induced by an adjacent dermoid cyst with occipital dermal sinus. METHODS: A 2-year-old girl presented with headache and vomiting. Physical examination showed nothing abnormal except for a small subcutaneous nodule above the occipital protuberance with a small skin opening. She had no neurological deficits. Neuroradiological studies including CT and MRI showed a cyst located in the posterior fossa. The cyst in the posterior fossa with occipital dermal sinus was diagnosed. She was treated by radical excision of the occipital cyst through a suboccipital approach, and was followed up. RESULTS: Histopathologic examination suggested a dermoid cyst with an abscess. Bacterial investigation revealed Staphylococcus epidermidis, and appropriate systemic antibiotic therapy was given. The child recovered and a 2-year follow-up was uneventful. CONCLUSIONS: Posterior fossa dermoid cyst should be considered in all children with occipital skin lesions, especially dermal sinus. CT and MRI scan are helpful in the diagnosis of the lesion. Neurosurgical treatment of the lesion should be planned early to prevent infections such as abscess and meningitis.

Poly[bis[aquaneodymium(III)]-mu2-oxalato-di-mu4-succinato].

In the title compound, [Nd(2)(C(4)H(4)O(4))(2)(C(2)O(4))(H(2)O)(2)](n), the flexible succinate anion assumes the gauche conformation and bridges the nine-coordinate Nd atoms to generate two-dimensional layers parallel to (010). The coordination polymer layers are linked into a three-dimensional framework by the rigid oxalate ligands. The oxalate ions are located on a center of inversion.

2,6-Bis[(2-hydroxy-3-methoxybenzylidene)hydrazinocarbonyl]pyridine monohydrate.

In the title compound, C(23)H(19)N(5)O(6).H(2)O, the two components are linked into complex chains by a combination of two independent O-H...O and two independent N-H...O hydrogen bonds. The complex chains are linked into a two-dimensional sheet network via pi-pi stacking interactions and C-H...O hydrogen bonds.

Tetra-kis(µ-propanoato-κO:O')bis-[(1,10-phenanthroline-κN,N')(propanoato-κO,O')samarium(III)].

The title complex, [Sm(2)(C(3)H(5)O(2))(6)(C(12)H(8)N(2))(2)], is a dinuclear centrosymmetric mol-ecule, in which two crystallographically equivalent Sm atoms, separated by 3.9502 (2) Å, are bridged by four propanoate anions. Each Sm atom is coordinated by two N atoms from one chelating phenanthroline ligand and seven carboxylate O atoms from five propanoate anions, to form a distorted tricapped trigonal prism.