Neuronal intranuclear inclusion disease (NIID) is a slowly progressive neurodegenerative disease characterized by eosinophilic hyaline intranuclear inclusions in the central and peripheral nervous system, and also in the visceral organs. Although in recent years skin biopsy is useful for the antemortem diagnosis of this disease, it is often misdiagnosed due to its highly variable clinical manifestations. A case of NIID is reported here. The patient had a long course of disease, mainly presenting as dysfunction of autonomic nervous system. No significant cognitive impairment was found. Thus, a new idea is provided for the diagnosis of this disease.

Objective:To explore the impact of domestic bivalirudin on platelet function during emergency percutane-ous coronary intervention (PCI) .Methods :A total of 100 patients with acute ST segment elevation myocardial in-farction who recieved emergency PCI were randomly divided into unfractionated heparin group (UFH group ,n=53) and bivalirudin group (n=47) .Adenyl diphosphoric acid (ADP)-induced platelet aggregation rate was meas-ured and statistically compared between two groups before and after PCI .Results:Before emergency PCI ,there was no significant difference in ADP-induced platelet aggregation rate between two groups (P=0.99) .After emergency PCI ,ADP-induced platelet aggregation rate in bivalirudin group was significantly lower than that of UFH group [ (16.46 ± 10.23)% vs .(25.21 ± 15.91) % , P<0.01] .Conclusion:During percutaneous coronary intervention , compared with routine heparin anticoagulation , bivalirudin , as an anticoagulant , can more significantly inhibit platelet aggregation and possess antiplatelet effect .

Langerhans cell histiocytosis (LCH) is a rare inflammatory myeloid neoplastic disease which is characterized by CD1a + /CD207 + dendritic cell proliferation.LCH can affect multiple systems, and the prevalence of central nervous system involved LCH (CNS-LCH) ranges from 3.4% to 57%.The pathogenesis of CNS-LCH remains unclear.CNS-LCH can be divided into the following: focal mass lesions and lesions associated with neurodegeneration (ND). The clinical manifestations of CNS-LCH vary greatly due to different involved organs.The hypothalamic pituitary-adrenal (HPA) axis is among the most commonly involved site in CNS-LCH with focal mass lesions, and HPA infiltration presents clinically as diabetes insipidus and deficiency of anterior pituitary hormone secretion.LCH-ND is a rare, long-term neurologic complication which can seriously affect patients′life quality.It is mainly characterized by neurological disorders and/or progressive imaging changes.The current standard treatment of CNS-LCH focal mass lesions is based on the Histiocyte Society LCHIII approach, while there is no established optimal therapy for patients who develop LCH-ND.The pathogenesis, clinical manifestations, diagnosis and treatment of CNS-LCH are briefly reviewed in this article in order to provide a reference for clinical diagnosis and treatment.

Vincristine, a widely used chemotherapeutic agent for treating different cancer, often induces severe peripheral neuropathic pain. A common symptom of vincristine-induced peripheral neuropathic pain is mechanical allodynia and hyperalgesia. However, mechanisms underlying vincristine-induced mechanical allodynia and hyperalgesia are not well understood. In the present study, we show with behavioral assessment in rats that vincristine induces mechanical allodynia and hyperalgesia in a PIEZO2 channel-dependent manner since gene knockdown or pharmacological inhibition of PIEZO2 channels alleviates vincristine-induced mechanical hypersensitivity. Electrophysiological results show that vincristine potentiates PIEZO2 rapidly adapting (RA) mechanically-activated (MA) currents in rat dorsal root ganglion (DRG) neurons. We have found that vincristine-induced potentiation of PIEZO2 MA currents is due to the enhancement of static plasma membrane tension (SPMT) of these cells following vincristine treatment. Reducing SPMT of DRG neurons by cytochalasin D (CD), a disruptor of the actin filament, abolishes vincristine-induced potentiation of PIEZO2 MA currents, and suppresses vincristine-induced mechanical hypersensitivity in rats. Collectively, enhancing SPMT and subsequently potentiating PIEZO2 MA currents in primary afferent neurons may be an underlying mechanism responsible for vincristine-induced mechanical allodynia and hyperalgesia in rats. Targeting to inhibit PIEZO2 channels may be an effective analgesic method to attenuate vincristine-induced mechanical hypersensitivity.

Parvalbumin interneurons belong to the major types of GABAergic interneurons. Although the distribution and pathological alterations of parvalbumin interneuron somata have been widely studied, the distribution and vulnerability of the neurites and fibers extending from parvalbumin interneurons have not been detailly interrogated. Through the Cre recombinase-reporter system, we visualized parvalbumin-positive fibers and thoroughly investigated their spatial distribution in the mouse brain. We found that parvalbumin fibers are widely distributed in the brain with specific morphological characteristics in different regions, among which the cortex and thalamus exhibited the most intense parvalbumin signals. In regions such as the striatum and optic tract, even long-range thick parvalbumin projections were detected. Furthermore, in mouse models of temporal lobe epilepsy and Parkinson's disease, parvalbumin fibers suffered both massive and subtle morphological alterations. Our study provides an overview of parvalbumin fibers in the brain and emphasizes the potential pathological implications of parvalbumin fiber alterations.
Mice ; Animals ; Epilepsy, Temporal Lobe/pathology* ; Parvalbumins/metabolism* ; Parkinson Disease/pathology* ; Neurons/metabolism* ; Interneurons/physiology* ; Disease Models, Animal ; Brain/pathology*