Publications by authors named "Zhi-Hao Lin"

Neuropathic pain is characterized by a high prevalence and associated with a variety of disorders of the peripheral and central nervous systems. It remains a major challenge for clinical management due to lack effective treatments. Our previous studies have demonstrated that nerve injury-induced neuroinflammation plays a critical role in regulating the development and maintenance of neuropathic pain.

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Background: Diabetic nephropathy (DN) is a microangiopathy of type 2 diabetes mellitus (T2DM), which can damage the kidney through various ways and mechanisms due to the nature of the disease, involving the renal interstitium and glomeruli. However, in the early stage of the disease, patients only showed kidney volume increase and glomerular hyperthyroidism, and typical symptoms that are difficult to arouse individual attention were noticed.

Aim: To observe the expression of serum retinol-binding protein (RBP) and urinary N-acetyl-β-D-glucosaminidase (NAG) in patients with DN, and to analyze their value in disease prediction, so as to provide new targets for early diagnosis and treatment of DN.

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DNA damage and defective DNA repair are extensively linked to neurodegeneration in Parkinson's disease (PD), but the underlying molecular mechanisms remain poorly understood. Here, we determined that the PD-associated protein DJ-1 plays an essential role in modulating DNA double-strand break (DSB) repair. Specifically, DJ-1 is a DNA damage response (DDR) protein that can be recruited to DNA damage sites, where it promotes DSB repair through both homologous recombination and nonhomologous end joining.

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Microglial hyperactivation of the NOD-, LRR-, and pyrin domain-containing 3 (NLRP3) inflammasome contributes to the pathogenesis of Parkinson's disease (PD). Recently, neuronally expressed NLRP3 was demonstrated to be a Parkin polyubiquitination substrate and a driver of neurodegeneration in PD. However, the role of Parkin in NLRP3 inflammasome activation in microglia remains unclear.

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Article Synopsis
  • - Mutations in the PRKN gene are a leading cause of autosomal recessive Parkinson's disease (PD), but research on parkin-/- mice shows no early loss of dopaminergic neurons or motor symptoms.
  • - This study focused on how the absence of the parkin gene affected the retina's mitochondria and synaptic structures in 6-month-old mice, revealing a thicker retina and significant mitochondrial abnormalities.
  • - The findings indicate that parkin-/- mice experienced impaired mitochondrial function and structural changes in the retina, which disrupted communication between photoreceptors and retinal neurons, leading to visual impairment.
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Ferroptosis, a novel form of regulated cell death, is caused by accumulation of lipid peroxides and excessive iron deposition. This process has been linked to the death of dopaminergic neurons in substantia nigra compacta (SNc) of Parkinson's disease (PD) patients. Quercetin (QCT), a natural flavonoid, has multiple pharmacological activities.

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Recent evidence suggests that innate and adaptive immunity play a crucial role in Parkinson's disease (PD). However, studies regarding specific immune cell classification in the peripheral blood in PD remain lacking. Therefore, we aimed to explore the different immune status in patients with PD at different ages of onset.

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Background: Emerging evidence indicates that the apolipoprotein E (APOE) ε4 exacerbates α-synuclein pathology.

Objective: To determine whether APOE ε4 contributes to motor progression in early Parkinson's disease (PD).

Methods: Longitudinal data were obtained from 384 patients with PD divided into APOE ε4 carriers (n = 85) and noncarriers (n = 299) in the Parkinson's Progression Marker Initiative.

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Background: To date, the genetic contribution to Parkinson's disease (PD) remains unclear. Mutations in the collagen type VI alpha 3 (COL6A3) gene were recently identified as a cause of isolated dystonia. Since PD and dystonia are closely related disorders with shared clinical and genetic characteristics, we explored the association between COL6A3 and PD in a Chinese cohort.

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Point clouds are among the popular geometry representations in 3D vision. However, unlike 2D images with pixel-wise layouts, such representations containing unordered data points which make the processing and understanding the associated semantic information quite challenging. Although a number of previous works attempt to analyze point clouds and achieve promising performances, their performances would degrade significantly when data variations like shift and scale changes are presented.

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Background: To date, several studies have suggested that genes involved in monogenic forms of Parkinson's disease (PD) contribute to unrelated sporadic cases, but there is limited evidence in the Chinese population.

Methods: We performed a systematic analysis of 12 autosomal-dominant PD (AD-PD) genes (SNCA, LRRK2, GIGYF2, VPS35, EIF4G1, DNAJC13, CHCHD2, HTRA2, NR4A2, RIC3, TMEM230, and UCHL1) using panel sequencing and database filtration in a case-control study of a cohort of 391 Chinese sporadic PD patients and unrelated controls. We evaluated the association between candidate variants and sporadic PD using gene-based analysis.

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Recently, the arylsulfatase A (ARSA) variant c.899 T > C (p.L300S) was identified to be segregated with Parkinson's disease (PD) in one family of Japanese descent.

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Despite some differences in clinical presentation, it is often difficult to differentiate between dementia with Lewy bodies (DLB), clinical Alzheimer's dementia (AD) and Parkinson's disease dementia. However, differentiation can be crucial, especially as patients with DLB characteristically have a hypersensitivity to most antiemetic and neuroleptic drugs as they affect the cholinergic and dopaminergic system, potentially leading to life-threatening catatonia, loss of cognitive function and muscle rigidity. The aim of this study is to evaluate if resting state (RS) functional MRI (fMRI) can be used in routine practice on a 1.

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