Association of lipid levels with motor and cognitive function and decline in Parkinson's disease.

BACKGROUND: Most studies have focused on comparing blood lipid biomarkers between Parkinson's disease (PD) and normal controls (NC). However, further research is necessary to explore the impact of blood lipid levels on motor and cognitive function, as well as the progression of motor dysfunction and cognitive decline over time. Thus, the aim of this study is to investigate the relationship between blood lipid biomarkers and these indicators in individuals with PD. METHODS: The cohort study enrolled 157 PD patients and 146 NC from the Tianjin Huanhu Hospital from September 2017 to September 2019. Serum lipid fractions were detected in fasting serum samples. PD patients were followed up at 2 ± 0.6 years for clinical assessment. RESULTS: PD patients exhibited lower serum triglyceride (TG) levels as compared to NC (P = 0.008). PD male patients exhibited lower serum lipoprotein cholesterol(LDL-C) and total cholesterol (TC) levels than female patients (LDL-C: P = 0.034; TC: P = 0.019). Serum TG levels correlated significantly with Unified PD Rating Scale III, Hoehn and Yahr stage and Montreal Cognitive Assessment scores in PD patients. Additionally, serum TG levels were associated with follow-up motor function decline and cognitive decline in adjusted regression models in PD patients. CONCLUSIONS: To summarise, the study findings suggest that decreased serum TG levels are significantly associated with greater motor dysfunction, cognitive dysfunction and the greater deterioration of the two indicators.

Advancing predictive markers in lung adenocarcinoma: A machine learning-based immunotherapy prognostic prediction signature.

The prognosis of lung adenocarcinoma (LUAD) is generally poor. Immunotherapy has emerged as a promising therapeutic modality, demonstrating remarkable potential for substantially prolonging the overall survival of individuals afflicted with LUAD. However, there is currently a lack of reliable signatures for identifying patients who would benefit from immunotherapy. We conducted a comparative analysis of two immunotherapy cohorts (OAK and POPLAR) and utilized single-factor COX regression to identify genes that significantly impact the prognosis of LUAD. Based on the TCGA-LUAD dataset, we employed a combination of 101 machine learning algorithms to construct a model and selected the optimal model. The model was validated on five GEO datasets and compared with 144 previously published signatures to assess its performance. Subsequently, we explored the underlying biological mechanisms through tumor mutation burden analysis, enrichment analysis, and immune infiltration analysis. An immunotherapy prognostic prediction signature (IPPS) was constructed based on 13 genes, showing robust performance in the TCGA-LUAD dataset. IPPS exhibited consistent predictive accuracy in the validation cohorts. Compared to 144 previously published signatures, IPPS consistently ranked among the top in terms of C-index values. Further exploration revealed differences between high and low-IPPS groups in terms of tumor mutation burden, pathway enrichment, and immune infiltration. IPPS demonstrates strong predictive capabilities for the prognosis of LUAD patients, offering the potential to identify suitable candidates for immunotherapy and contribute to precision treatment strategies for LUAD.

Cancer associated fibroblasts-derived SULF1 promotes gastric cancer metastasis and CDDP resistance through the TGFBR3-mediated TGF-ß signaling pathway.

SULF1 has been implicated in a number of malignancies. The function of SULF1 in gastric cancer is disputed. The objective of this study was to examine the role and underlying molecular mechanisms of SULF1 in the context of gastric cancer. We found that the expression of SULF1 was increased in gastric cancer, especially in cancer-associated fibroblasts. The overexpression of SULF1 was found to be significantly correlated with unfavorable prognosis among individuals diagnosed with gastric cancer. Functionally, cancer-associated fibroblasts-derived SULF1 served as a oncogenic molecule which facilitated gastric cancer cells metastasis and CDDP resistance. Mechanistically, SULF1 regulated the communication between gastric cancer cells and cancer-associated fibroblasts in tumor microenvironment as a signaling molecule. Cancer-associated fibroblasts-secreted SULF1 interfered with the interaction between TGF-ß1 and TGFBR3 by combining with TGFBR3 on gastric cancer cell membrane, subsequently activated TGF-ß signaling pathway. In conclusion, our findings have presented novel approaches for potential treatment and prognosis prediction in individuals diagnosed with gastric cancer through the targeting of the CAFs-SULF1-TGFBR3-TGF-ß1 signaling axis.

Unveiling the oncogenic role of CLDN11-secreting fibroblasts in gastric cancer peritoneal metastasis through single-cell sequencing and experimental approaches.

BACKGROUND: Fibroblasts are necessary to the progression of cancer. However, the role of fibroblasts in peritoneal metastasis (PM) of gastric cancer (GC) remains elusive. In this study, we would explore the role of fibroblasts mediated cell interaction in PM of GC. METHODS: Single-cell sequencing data from public database GSE183904 was used to explore the specific fibroblast cluster. Fibroblasts were extracted from PM and GC tissues. The expression level of CXCR7 was verified by western blot, immunohistochemistry. The role of CLDN11 was investigate through in vitro and in vivo study. Multiple immunohistochemistry was used to characterize the tumor microenvironment. RESULTS: CXCR7-positive fibroblasts were significantly enriched in PM of GC. CXCR7 could promote the expression of CLDN11 through activation of the AKT pathway in fibroblasts. Fibroblasts promote the GC proliferation and peritoneal metastasis by secreting CLDN11 in vitro and in vivo. Furthermore, it was revealed that CXCR7-positive fibroblasts were significantly associated with M2-type macrophages infiltration in tissues. CONCLUSION: CXCR7-positive fibroblasts play an essential role in PM of GC via CLDN11. Therapy targeting CXCR7-positive fibroblasts or CLDN11 may be helpful in the treatment of GC with PM.

A Sn-Based Hybrid Ferroelastic Semiconductor with High-Temperature Dielectric Switching.

Organic-inorganic halide hybrids have been extensively developed and used in optoelectronic devices because of their superior performance such as ease of assembly, flexible structural tunability, and excellent optoelectronic properties. Ferroelastic strain might be used to modulate and control photoelectric properties such as photovoltaic voltage, while organic-inorganic hybrid ferroelastic semiconductors remain relatively unexplored. Herein, we successfully design a new Sn-base, lead-free hybrid ferroelastic semiconductor, [TPMA]2[SnCl6] (TPMA = benzyl trimethylammonium). It undergoes a high-temperature -3mF-1-type ferroelastic phase transition at 408 K, and intriguingly, its ferroelastic domains can be simultaneously switched under the stimulation of external heat and stress. The ferroelastic phase transition might be derived from the order-disorder transition of organic cations during heating and cooling. Moreover, [TPMA]2[SnCl6] also demonstrates a high-temperature dielectric switching property around 408 K, which has good stability and reproducibility. With those benefits, [TPMA]2[SnCl6] shows great potential in applications such as energy storage devices, optoelectronic devices, shape memory, intelligent switches, and so on.

H3K27 acetylation activated-PDLIM7 promotes castration-resistant prostate cancer progression by inducing O-Glycosylation of YAP1 protein.

Castration-resistant prostate cancer (CRPC) is a fatal disease that evolves from prostate cancer due to drug resistance after long-term androgen deprivation therapy. In this study, we aimed to find novel molecular targets for treating CRPC. Through peptidome, we screened out polypeptides dysregulated in the serum of CRPC patients. According to RT-qPCR analysis and cell viability detection, we chose PDZ and LIM Domain 7 (PDLIM7) as the research object. As demonstrated by loss-of-function assays, silencing of PDLIM7 could suppress CRPC cell proliferation, migration, and angiogenesis. Moreover, PDLIM7 knockdown enhanced the sensitivity of CRPC cells to docetaxel treatment. Subsequently, we found that CBP/p300 increases the H3K27ac level in the PDLIM7 promoter to activate PDLIM7. Mechanism experiments such as IP and western blot revealed that PDLIM7 interacted with YAP1 to induce O-Glycosylation of YAP1 and thus stabilize YAP1 protein. Rescue assays demonstrated that PDLIM7 promoted the malignant processes of CRPC cells through YAP1. Finally, an animal study validated that PDLIM7 aggravated tumor growth. In conclusion, our findings highlighted the oncogenic role of PDLIM7 upregulated by CBP/p300-induced H3K27ac enhancement in CRPC by stabilizing YAP1.

Case report: De novo variant of SETD1A causes infantile epileptic spasms syndrome.

Infantile epileptic spasms syndrome (IESS) is one of the most common epileptic encephalopathies of infancy, with typical clinical features defined by a triad of epileptic spasms, hypsarrhythmia, and developmental delay. Genetic factors are important causes of IESS. The SETD1A (SET Domain Containing 1A) gene encodes a histone lysine methyltransferase that activates gene transcription through histone H3 lysine K4 methylation. Mutations in the SETD1A gene have been associated with schizophrenia, and some have been reported to cause seizures. Herein, we report a case of IESS caused by a SETD1A gene mutation. Video electroencephalography showed hypsarrhythmia. No specific findings were obtained after brain MRI and metabolic work-up. The seizures disappeared after treatment with adrenocorticotropic hormone, vitamin B6, and valproic acid during hospitalization. Genetic testing revealed that the child had a variant (NM_014712.3:c.3005_3,006 delAG, p.Glu1002Glyfs*20) in exon 12 of the SETD1A gene, representing a de novo mutation. There have been no previous reports on the SETD1A gene causing infantile spasms. We also summarize the existing literature on SETD1A gene-related epilepsy to provide a reference for clinical diagnosis and treatment.

A novel PSMA targeted dual-function near-infrared fluorescence and PET probe for the image-guided surgery and detection of prostate cancer.

PURPOSE: Prostate-specific membrane antigen (PSMA) is a promising diagnostic biomarker for prostate cancer (PCa). NYM016, a novel small-molecule PSMA-targeted fluorescence probe for the surgical navigation of PCa, was designed in this work. Furthermore, the potential of the PET agent [68Ga]Ga-NYM016 for the radionuclide imaging of PCa was evaluated. METHODS: NYM016 was designed with the near-infrared fluorescent group Cyanine 7 (Cy7) and the chelating group NOTA. The radioactive probe [68Ga]Ga-NYM016 was designed and synthesized on the basis of NYM016. The abovementioned probes were assessed in PSMA-positive xenograft-bearing models and patients diagnosed with PCa. RESULTS: NYM016 obviously aggregated in the tumor site of the mouse model, and its fluorescence intensity was stable within 24 h. NYM016 was well-tolerated, and no adverse events were found in the clinical study. Moreover, it was also observed in the excised lesions from the patient with PCa, and its fluorescence aggregated at the same site where PSMA was highly expressed. In addition, the PSMA xenograft demonstrated intense [68Ga]Ga-NYM016 uptake at 2.5 min after injection. At 3 h after injection, [68Ga]Ga-NYM016 uptake by the PSMA xenograft gradually increased to 6.40 ± 0.19%ID/g, which was higher that by the blocked and negative groups (2.28 ± 0.07%ID/g, P < 0.05; 2.28 ± 0.22%ID/g, P < 0.05). In the clinical study, [68Ga]Ga-NYM016 was well-tolerated and no adverse events were observed. Substantial accumulation was observed in primary and metastatic lesions in a patient with recurrence with the maximum standardized uptake value of 18.93. Meanwhile, negative [68Ga]Ga-NYM016 uptake was observed at the prostate site of a patient with prostatitis. CONCLUSION: The novel fluorescence probe NYM016 and the radioactive tracer [68Ga]Ga-NYM016 are promising candidates for the surgical navigation and radionuclide imaging of PCa, respectively. TRIAL REGISTRATION: The clinical evaluation of this study was registered at Clinicaltrial.gov (NCT05623878) on 21 Dec, 2022.

The Abnormal Alternations of Brain Imaging in Patients with Chronic Obstructive Pulmonary Disease: A Systematic Review.

Background: Cognitive impairment (CI) is an important extrapulmonary complication in patients with chronic obstructive pulmonary disease (COPD). Multimodal Neuroimaging Examination can display changes in brain structure and functions in patients with COPD. Objective: The purpose of this systematic review is to provide an overview of the variations in brain imaging in patients with COPD and their potential relationship with CI. Furthermore, we aim to provide new ideas and directions for future research. Methods: Literature searches were performed using the electronic databases PubMed, Scopus, and ScienceDirect. All articles published between January 2000 and November 2021 that met the eligibility criteria were included. Results: Twenty of the 23 studies focused on changes in brain structure and function. Alterations in the brain's macrostructure are manifested in the bilateral frontal lobe, hippocampus, right temporal lobe, motor cortex, and supplementary motor area. The white matter microstructural changes initially appear in the bilateral frontal subcortical region. Regarding brain function, patients with COPD exhibited reduced frontal cerebral perfusion and abnormal alterations in intrinsic brain activity in the bilateral posterior cingulate cortex, precuneus, right lingual gyrus, and left anterior central gyrus. Currently, there is limited research related to brain networks. Conclusion: CI in patients with COPD may present as a type of dementia different from Alzheimer's disease, which tends to manifest as frontal cognitive decline early in the disease. Further studies are required to clarify the neurobiological pathways of CI in patients with COPD from the perspective of brain connectomics based on the whole-brain system in the future.

Clinical implications and mechanism of complement C1q in polymyositis.

Polymyositis (PM) is the most common autoimmune disease in neurology and among muscle disorders; it is of great significance to thoroughly understand the mechanism of PM to find new diagnosis and treatment methods. This research intends to elucidate the clinical implications and mechanisms of complement C1q in polymyositis (PM). One hundred fifteen PM patients (research group, RG) and 120 healthy subjects (control group, CG) who visited our hospital between March 2017 and March 2020 were selected. Peripheral blood C1q and creatine kinase (CK) levels of both groups were measured, and their correlations with clinical symptoms and prognostic recurrence of PM. Additionally, to further understand the mechanism of action of C1q in PM, we purchased BALB/c mice and grouped them as follows: control group with normal feeding, PM group with PM modeling, intervention group with PM modeling, and intraperitoneal injection of gC1qR monoclonal antibody 60.11, a C1q protein receptor. Inflammatory factors and muscle histopathology were detected in all groups of mice. Finally, rat macrophages (mø) were isolated, and changes in the biological behavior of mø were observed after silencing the expression of gC1qR. Serum C1q and CK were both higher in RG than in CG, with favorable diagnostic effects on PM (P < 0.05). C1q and CK increased in symptomatic anti-ribonuclear protein antibody (RNP)-positive patients but decreased in anti Jo-1 antibody (Jo-1)- and anti-neutrophil cytoplasmic antibody (ANCA)-positive patients (P < 0.05). PM mice were observed with elevated gC1qR, while model mice exhibited severe infiltration of inflammatory cells in muscle tissue, increased pro-IFs, and reduced anti-IFs, and the animals in the intervention group showed improved conditions (P < 0.05). Finally, it was found that CD68, CD86 protein, and invasion capacity of gC1qR-sh-transfected cells decreased, while CD206 and CD163 increased (P < 0.05). C1q is elevated in PM and is strongly linked to the pathological process of PM. Inhibition of gC1qR expression reduced inflammatory infiltration in PM mice.

Estrogen increases the expression of BKCa and impairs the contraction of colon smooth muscle via upregulation of sphingosine kinase 1.

Estrogen (E2) may impair the contraction of colonic smooth muscle (SM) leading to constipation. Large conductance Ca2+ -activated K+ channels (BKCa ) are widely expressed in the smooth muscle cells (SMCs) contributing to hyperpolarization and relaxation of SMCs. Sphingosine kinase 1 (SphK1) is known to influence the expression of BKCa . We aimed to elucidate the potential underlying molecular mechanism of BKCa and SphK1 that may influence E2-induced colonic dysmotility. In ovariectomized rats, SM contraction and expression of BKCa , SphK1, sphingosine-1-phosphate receptor (S1PR) were analyzed after the treatment with vehicle, BSA-E2, E2, and E2 receptor antagonist. The role of BKCa , SphK1, and S1PR in E2-induced SM dysmotility was investigated in rat colonic SMCs. The effect of SphK1 on SM contraction as well as on the expression of BKCa and S1PR was analyzed in SphK1 knock-out mutant mice and wild-type (WT) mice treated with or without E2. The E2-treated group exhibited a weak contraction of colonic SM and a delayed colonic transit. The treatment with E2 significantly upregulated the expression of BKCa , SphK1, S1PR1, and S1PR2, but not S1PR3, in colon SM and SMCs. Inhibition of BKCa , SphK1, S1PR1, and S1PR2 expression attenuated the effect of E2 on Ca2+ mobilization in rat colon SMCs. WT mice treated with E2 showed impaired gastrointestinal motility and enhanced expression of BKCa , S1PR1, and S1PR2 compared with those without E2 treatment. Conversely, in SphK1 knock-out mice treated with E2, these effects were partially reversed. E2 increased the release of S1P which in turn could have activated S1PR1 and S1PR2. Loss of SphK1 attenuated the effect of E2 on the upregulation of S1PR1 and S1PR2 expression. These findings indicated that E2 impaired the contraction of colon SM through activation of BKCa via the upregulation of SphK1 and the release of S1P. In the E2-induced BKCa upregulation, S1PR1 and S1PR2 might also be involved. These results may provide further insights into a therapeutic target and optional treatment approaches for patients with constipation.

Disconnection of Network Hubs Underlying the Executive Function Deficit in Patients with Ischemic Leukoaraiosis.

BACKGROUND: Cognitive impairment is the most common clinical manifestation of ischemic leukoaraiosis (ILA), but the underlying neurobiological pathways have not been well elucidated. Recently, it was thought that ILA is a "disconnection syndrome". Disorganized brain connectome were considered the key neuropathology underlying cognitive deficits in ILA patients. OBJECTIVE: We aimed to detect the disruption of network hubs in ILA patients using a new analytical method called voxel-based eigenvector centrality (EC) mapping. METHODS: Subjects with moderate to severe white matters hyperintensities (Fazekas score ≥3) and healthy controls (HCs) (Fazekas score = 0) were included in the study. The resting-state functional magnetic resonance imaging and the EC mapping approach were performed to explore the alteration of whole-brain network connectivity in ILA patients. RESULTS: Relative to the HCs, the ILA patients exhibited poorer cognitive performance in episodic memory, information processing speed, and executive function (all ps < 0.0125). Additionally, compared with HCs, the ILA patients had lower functional connectivity (i.e., EC values) in the medial parts of default-mode network (i.e., bilateral posterior cingulate gyrus and ventral medial prefrontal cortex [vMPFC]). Intriguingly, the functional connectivity strength at the right vMPFC was positively correlated with executive function deficit in the ILA patients. CONCLUSION: The findings suggested disorganization of the hierarchy of the default-mode regions within the whole-brain network in patients with ILA and advanced our understanding of the neurobiological mechanism underlying executive function deficit in ILA.

Brain glucose metabolism on [18F]-FDG PET/CT: a dynamic biomarker predicting depression and anxiety in cancer patients.

Objectives: To explore the correlation between the incidence rates of depression and anxiety and cerebral glucose metabolism in cancer patients. Methods: The experiment subjects consisted of patients with lung cancer, head and neck tumor, stomach cancer, intestinal cancer, breast cancer and healthy individuals. A total of 240 tumor patients and 39 healthy individuals were included. All subjects were evaluated by the Hamilton depression scale (HAMD) and Manifest anxiety scale (MAS), and were examined by whole body Positron Emission Tomography/Computed Tomography (PET/CT) with 18F-fluorodeoxyglucose (FDG). Demographic, baseline clinical characteristics, brain glucose metabolic changes, emotional disorder scores and their relations were statistically analyzed. Results: The incidence rates of depression and anxiety in patients with lung cancer were higher than those in patients with other tumors, and Standard uptake values (SUVs) and metabolic volume in bilateral frontal lobe, bilateral temporal lobe, bilateral caudate nucleus, bilateral hippocampus, left cingulate gyrus were lower than those in patients with other tumors. We also found that poor pathological differentiation, and advanced TNM stage independently associated with depression and anxiety risk. SUVs in the bilateral frontal lobe, bilateral temporal lobe, bilateral caudate nucleus, bilateral hippocampus, left cingulate gyrus were negatively correlated with HAMD and MAS scores. Conclusion: This study revealed the correlation between brain glucose metabolism and emotional disorders in cancer patients. The changes in brain glucose metabolism were expected to play a major role in emotional disorders in cancer patients as psychobiological markers. These findings indicated that functional imaging can be applied for psychological assessment of cancer patients as an innovative method.

Heat shock protein 90 C-terminal inhibitor PNSA promotes anticancer immunology of CD8+ T cells.

Penisuloxazin A (PNSA), a new compound from the fungus, is a novel C-terminal Hsp90 inhibitor reported by us before. It has been reported to possess antitumor activity and suppresses metastasis of breast cancer cells. However, the influence of PNSA on T cells is not fully understood. Here, we found that PNSA was much less toxic to lymphocytes than to tumor cells and it had no significant effect on populations of CD3+, CD4+ and CD8+ T lymphocytes. We discovered that PNSA directly enhanced the killing capacities of the CD8+ T and CD3+CD25- to CT26 cells, but not that of CD3+ cells due to the increase of Treg cells. What's more, PNSA pretreated tumor cells increase the sensitivity to CD8+ T cells mainly through the degradation of client protein of Hsp90 and declination of PD-L1 expression. Eventually, PNSA enhanced the killing ability of CD8+ and CD3+ T cells by simultaneously acting on lymphocytes and cancer cells. In vivo experiments, PNSA exhibited inhibition effects in the colon adenocarcinoma with increase of CD8 T cell infiltration in tumor tissues. All these results indicate that the novel Hsp90 C-terminal inhibitor-PNSA can promote lytic T cell immunological function to improve anticancer effect of PNSA, which provides a better foundation for anticancer drug development of PNSA in future.

Blood Neurofilament Light Chain in Different Types of Dementia.

AIMS: The study aimed to evaluate diagnostic values of circulating neurofilament light chain (NFL) levels in different types of dementia. BACKGROUND: Previous studies reported inconsistent change of blood NFL for different types of dementia, including Alzheimer's disease (AD), frontotemporal dementia (FTD), Parkinson's disease dementia (PDD) and Creutzfeldt-Jakob disease (CJD) and Lewy body dementia (LBD). OBJECTIVE: Meta-analysis was conducted to summarize the results of studies evaluating diagnostic values of circulating NFL levels in different types of dementia to enhance the strength of evidence. METHODS: Articles evaluating change in blood NFL levels in dementia and published before July 2022 were searched on the following databases (PubMed, Web of Science, EMBASE, Medline and Google Scholar). The computed results were obtained by using STATA 12.0 software. RESULTS: AD patients showed increased NFL concentrations in serum and plasma, compared to healthy controls (HC) (standard mean difference (SMD) = 1.09, 95% confidence interval (CI): 0.48, 1.70, I2 = 97.4%, p < 0.001). In AD patients, higher NFL concentrations in serum and plasma were associated with reduced cerebrospinal fluid (CSF) Aß1-42, increased CSF t-tau, increased CSF p-tau, reduced Mini-Mental State Examination (MMSE) and decreased memory. Additionally, mild cognitive impairment (MCI) showed elevated NFL concentrations in serum and plasma, compared to HC (SMD = 0.53, 95% CI: 0.18, 0.87, I2 = 93.8%, p < 0.001). However, in MCI, no significant association was found between NFL concentrations in serum, plasma and memory or visuospatial function. No significant difference was found between preclinical AD and HC (SMD = 0.18, 95% CI: -0.10, 0.47, I2 = 0.0%, p = 0.438). FTD patients showed increased NFL concentrations in serum and plasma, compared to HC (SMD = 1.08, 95% CI: 0.72, 1.43, I2 = 83.3%, p < 0.001). Higher NFL concentrations in serum and plasma were associated with increased CSF NFL in FTD. Additionally, the pooled parameters calculated were as follows: sensitivity, 0.82 (95% CI: 0.72, 0.90); specificity, 0.91 (95% CI: 0.83, 0.96). CJD patients showed increased NFL concentrations in serum and plasma, compared to HC. No significant difference in NFL level in serum and plasma was shown between AD and FTD (SMD = -0.03, 95% CI: -0.77, 0.72, I2 = 83.3%, p = 0.003). CONCLUSION: In conclusion, the study suggested abnormal blood NFL level in AD and MCI, but not in preclinical AD. FTD and CJD showed abnormal blood NFL levels.

Generation of bright-dark solitons in an Er-doped fiber laser employing InSb as a saturable absorber.

In this paper, an indium antimonide (InSb) saturable absorber (SA) was successfully fabricated. The saturable absorption properties of the InSb SA were studied, and they show a modulation depth and a saturable intensity of 5.17% and 9.23M W/c m 2, respectively. By employing the InSb SA and building the ring cavity laser structure, the bright-dark soliton operations were successfully obtained by increasing the pump power to 100.4 mW and adjusting the polarization controller. As the pump power increased from 100.4 to 180.3 mW, the average output power increased from 4.69 to 9.42 mW, the corresponding fundamental repetition rate was 2.85 MHz, and the signal-to-noise ratio was 68 dB. The experimental results show that InSb with excellent saturable absorption characteristics can be used as a SA to obtain pulse lasers. Therefore, InSb has important potential in fiber laser generation, further applications in optoelectronics, laser distance ranging, and optical fiber communication, and it can be widely developed.

Simultaneous detection of five viruses and two viroids affecting apples through a DNA macroarray chip.

Multiple infections of various viruses and viroids in apple trees are common and have caused a significant loss in the world apple industry. To provide an early detection of any of those possible pathogens at the molecular level, a multiplex DNA macroarray chip was designed and developed for a simultaneous identification of five common apple viruses and two viroids including apple chlorotic leaf spot virus (ACLSV), apple stem pitting virus (ASPV), apple stem grooving virus (ASGV), apple mosaic virus (ApMV), apple necrosis mosaic virus (ApNMV), apple scar skin viroid (ASSVd), and apple dimple fruit viroid (ADFVd). The macroarray with a 23 bp probe arranged with the coat protein (CP) gene or a target DNA segment of each viruses and viroids has demonstrated a high specificity and sensitivity without any competitions, inhibitions or cross-interferences when it was tested against more than a mixture of viral and viroid samples. To our best knowledge, this is the first report on the simultaneous detection of five different apple viruses and two viroids through using a DNA macroarray, therefore, we suggest that this detection protocol and procedure be used for any apple viral diagnosis before setting up a production nursery for virus-free apple seedlings.

Functional brain alterations in migraine patients: an activation likelihood estimation study.

BACKGROUND: Previous functional magnetic resonance imaging (fMRI) studies reported inconsistent results for comparison in brain activation between migraine patients and healthy controls (HC). Thus, activation likelihood estimation (ALE) method, a powerful voxel-based technique, was used to explore the concordant functional brain changes in migraine patients. METHODS: Studies published before October 2022 were searched in the following databases (PubMed, Web of Science and Google Scholar). RESULTS: Migraine without aura (MWoA) patients showed reduced amplitude of low-frequency fluctuations (ALFF) in right lingual gyrus, the left posterior cingulate and the right precuneus (PCUN), compared to HC. Migraine patients showed increased ALFF in the right claustrum, the left caudate, the left insula and the right parahippocampal gyrus, compared to HC. MWoA patients showed reduced regional homogeneity (ReHo) in the right culmen, compared to HC. In addition, migraine patients showed increased ReHo in the bilateral thalamus, compared to HC. MWoA patients showed reduced whole-brain functional connectivity (FC) in the left middle occipital gyrus and the right superior parietal lobule, compared to HC. In addition, migraine patients showed increased whole-brain FC in the left middle temporal gyrus (MTG), the right inferior frontal gyrus, the right superior temporal gyrus (STG) and the left inferior temporal gyrus, compared to HC. CONCLUSIONS: ALE analysis identified consistent functional changes in widespread regions, especially in cingulate gyrus, basal ganglia region and frontal cortex in migraine. These regions involve in pain processing, cognitive dysfunction and emotional problems. These results may provide important clues for clarifying the pathophysiology of migraine.

Predicting cerebral white matter lesions based on the platelet-to-white blood cell ratio in hypertensive patients.

Hypertension is a common chronic disease affecting many people. White matter lesions (WMLs) are one of the imaging features of cerebrovascular disease. Predicting the possibility of developing syncretic WMLs in patients with hypertension may contribute to the early identification of serious clinical conditions. This study aims to build a model to identify patients who suffered from moderate-to-severe WMLs by using recognized WMLs risk factors including age and history of diabetes and a new factor named platelet-to-white blood cell ratio (PWR). A total of 237 patients were included in this study. The Affiliated ZhongDa Hospital of Southeast University Research Ethics Committee approved this study (Ethics No. 2019ZDSYLL189-P01). We developed a nomogram to predict the risk of syncretic WMLs in patients with hypertension using the above factors. Higher total scores on the nomogram indicated a higher risk of syncretic WMLs. This means older age, smaller PWR, and patients suffering from diabetes contributed to a greater chance for the patient to suffer from syncretic WMLs. We used a decision analysis curve(DCA) to determine the net benefit of the prediction model. The DCA we constructed showed that using our model to decide whether patients suffered from syncretic WMLs or not was better than assuming they all suffered from syncretic WMLs or all WMLs-free. As a result, the area under the curve of our model was 0.787. By integrating PWR, history of diabetes, and age, we could estimate integrated WMLs in hypertensive patients. This study provides a potential tool to identify cerebrovascular disease in patients with hypertension.

Soluble TREM2 in body fluid in Alzheimer's disease and Parkinson's disease.

BACKGROUND: Previous studies showed conflicting results regarding soluble triggering receptor expressed on myeloid cells 2 (sTREM2) level alteration in body fluid in Alzheimer's disease (AD) and Parkinson's disease (PD). METHODS: We applied the STATA 12.0 software to compute standard mean difference (SMD) and 95% confidence interval (CI). RESULTS: The study showed elevated sTREM2 level in cerebrospinal fluid (CSF) in AD, mild cognitive impairment (MCI), and preclinical AD (pre-AD) patients, compared to healthy controls (HCs) with random effects models (AD: SMD 0.28, 95% CI 0.12 to 0.44, I2 = 77.6%, p < 0.001; MCI: SMD 0.29, 95% CI 0.09 to 0.48, I2 = 89.7%, p < 0.001; pre-AD: SMD 0.24, 95% CI 0.00 to 0.48, I2 = 80.8%, p < 0.001). The study showed no significant difference in sTREM2 level in plasma between AD patients and HCs with a random effects model (SMD 0.06, 95% CI - 0.16 to 0.28, I2 = 65.6%, p = 0.008). The study showed no significant difference in sTREM2 level in CSF or plasma between PD patients and HCs with random effects models (CSF: SMD 0.33, 95% CI - 0.02 to 0.67, I2 = 85.6%, p < 0.001; plasma: SMD 0.37, 95% CI - 0.17 to 0.92, I2 = 77.8%, p = 0.011). CONCLUSIONS: In conclusion, the study highlighted the CSF sTREM2 as a promising biomarker in the different clinical stages of AD. More studies were essential to explore the CSF and plasmatic concentrations of sTREM2 alteration in PD.