Objective: With the development of extracellular vesicles (EVs) based on stem cells research all over the world, our present study was aiming to discover the global trends in this field. Methods: All publications related to EVs based on stem cells from 1991 to 2021 were collected from the Science Citation Index-Expanded of Web of Science Subsequently, the data were evaluated using the bibliometric methodology. In terms of visualized study, the VOS viewer software was performed to investigate the bibliographic coupling, co-citation, co-authorship, and co-occurrence trends, and last for the publication's trends involved in the field of EVs based on stem cells. Results: A total of 8,208 publications were retrieved and the relative number of global publications and research interests were increasing every year especially in recent 5 years. China rank top one in terms of total publications, prolific authors, and funds, whereas the USA made the greatest contributions with the most total citations and highest H-index to the global research. Stem cell research therapy contributed the highest publications, whereas the journal of PLOS ONE showed the best total link strength. The Shanghai Jiao Tong University, University of California System, and Harvard University were the most contributive institutions. The global studies could be divided into six clusters as follows: cancer research, musculoskeletal system research, respiratory system research, urinary system and endocrine system research, nerve system research, and cardiovascular system research. All the directions were predicted to still hotspots in near future researches in this field. Conclusion: The total number of publications about EVs based stem cells would be increasing according to the current global trends. China and the USA was the largest contributors in this field. Further efforts should be put in the directions of cancer research, musculoskeletal system research, respiratory system research, urinary system and endocrine system research, nerve system research, as well was cardiovascular system research in this field of EVs based stem cells.

SUMMARYSleep is a ubiquitous behavior in animal species. Yet, brain circuits controlling sleep remain poorly understood. Previous studies have identified several brain structures that promote sleep, but whether these structures are involved in sleep initiation or sleep maintenance remains largely unknown. Here we identified a population of glutamatergic neurons in the medulla that project to the preoptic area (POA), a prominent sleep-promoting region. Chemogenetic silencing of POA-projecting medulla neurons disrupts the transitions from wakefulness to Non-Rapid Eye Movement (NREM) sleep, whereas chemogenetic activation of these neurons promotes NREM sleep. Moreover, we show that optogenetic activation of medulla glutamatergic neurons or their projections in the POA reliably initiates long-lasting NREM sleep in awake mice. Together, our findings uncover a novel excitatory brainstem-hypothalamic circuit that controls the wake-sleep transitions.

Osteoarthritis (OA) is a degenerative joint disease that affects the entire joint and has been a tremendous burden on the health care system worldwide. Although cell therapy has made significant progress in the treatment of OA and cartilage regeneration, there are still a series of problems. Recently, more and more evidence shows that extracellular vesicles (EVs) play an important role in the progression and treatment of OA. Here, we discuss that EVs from different cell sources not only participate in OA progression, but can also be used as effective tools for the diagnosis and treatment of OA. In addition, cell pretreatment strategies and EV tissue engineering play an increasingly prominent role in the field of OA treatment. This article will systematically review the latest developments in these areas. As stated above, it may provide new insights for improving OA and cartilage regeneration.

Articular cartilage (AC) damage is quite common, but due to AC’s poor self-healing ability, the damage can easily develop into osteoarthritis (OA). To solve this problem, we developed a microsphere/hydrogel system that provides two growth factors that promote cartilage repair: transforming growth factor-β3 (TGF-β3) to enhance cartilage tissue formation and ghrelin synergy TGF-β to significantly enhance the chondrogenic differentiation. The hydrogel and microspheres were characterized in vitro, and the biocompatibility of the system was verified. Double emulsion solvent extraction technology (w/o/w) is used to encapsulate TGF-β3 and ghrelin into microspheres, and these microspheres are encapsulated in a hydrogel to continuously release TGF-β3 and ghrelin. According to the chondrogenic differentiation ability of mesenchymal stem cells (MSCs) in vitro, the concentrations of the two growth factors were optimized to promote cartilage regeneration.

A multinucleon transfer and cluster-decay experiment, namely 9Be(13C,18O∗→14C+α)α, was performed at a beam energy of 65 MeV. Resonant states in 18O from 7 to 19 MeV, including some newly observed ones, are reconstructed with high resolution, based on the coincident detection of various combinations of the final fragments. The α-decay branching ratios for 14 states are extracted from both the invariant-mass and the missing-mass measurements. Angular correlation analysis was conducted for the 10.3-MeV (4+) state. The present work supports the existence of the positive-parity rotational band associated with the 14C+α molecular structure in 18O, but the negative-parity band members were not identified.1 MoreReceived 24 February 2019Revised 3 May 2019DOI:https://doi.org/10.1103/PhysRevC.99.064315©2019 American Physical SocietyPhysics Subject Headings (PhySH)Research AreasAlpha decayCluster modelsNuclear structure & decaysTransfer reactionsProperties6 ≤ A ≤ 19Nuclear Physics

FK506 binding protein 12.6 (FKBP12.6), a protein that binds to and regulates the ryanodine receptor type 2 (RyR2) Ca2+ release channels, may act as an important regulator of catecholamine secretion. In the present study, the role of FKBP12.6 in the control of chromaffin cell exocytosis has been investigated using FKBP12.6-null mice. The results showed that FKBP12.6 was expressed in mouse chromaffin cells; deletion of FKBP12.6 did not change the depolarization induced Ca2+ current and exocytosis. However, deletion of FKBP12.6 resulted in an enhanced caffeine-induced global Ca2+ transient and larger caffeine-induced exocytosis in chromaffin cells of mice. These results indicate that FKBP12.6 is involved in catecholamine secretion through regulation of Ca2+ release channel in mouse chromaffin cells.

Parkinson's disease (PD) is a neurodegenerative disorder due to reduced dopamine (DA) in the striatum and loss of DA neurons in the substantia nigra pars compacta. Embryonic stem cells (ESCs) are an optimal source for cell therapy for PD. We recently developed a fast (one-week) protocol using small molecules that effectively induces human ESCs to become primitive neural stem cells (pNSCs), which are then differentiated into DA-like neurons in vitro. As pNSCs are infinitely expandable, this approach offers a strategy to readily generate DA neurons on a large scale. But whether these pNSC-differentiated DA (pNSC-DA) neurons can functionally integrate into the damaged brain is unknown. Here, we transplanted pNSC-DA neurons into 6-hydroxydopamine-induced rat models of PD and monitored their behavior for 16 weeks. In striatum in vivo, we first determined that the grafted pNSC-DA neurons secreted DA(using HPLC with a 200-μm microdialysis probe at a sampling rate of 0.002 Hz); then we recorded DA release by electrochemical amperometry (using a 7-μm carbon-fiber electrode at a sampling rate of 1000 Hz), showing that the grafted pNSC-DA neurons significantly rescued DA release in slices (7%) and in vivo (16%). Furthermore, the transplanted cells survived for at least 16 weeks and dramatically rescued the apomorphine-induced asymmetric rotation behavior in PD rats. Thus, we draw the conclusion that transplanted pNSC-DA neurons can functionally integrate into the brain and partially relieve Parkinsonian symptoms in rats. Our work provides direct evidence for a therapeutic role of pNSC-DA neurons in treating Parkinsonian syndrome.

Objective To investigate the technical methods for culturing and purifying the olfactory ensheathing cells(OECs) from the adult canine and human olfactory epithclium.To establish a basis for future studying the transplantation of peripheral(OECs) to repair the spinal cord injury in human. Methods Purifying the OECs from the olfactory epithelium of adult canine and man according to their different attachment time with other types of cells.Culturing for 25 days,observed at 6d,10d and 25d,and immunostained with NGFRp75 antibody to identify the OECs. Results The number of cultured olfactory epithelium OECs from both adult canine and man were increased much more after 10 days of culture,and its sharp showed to be bi-polar or tripe-polar and are immunopositive to NGFRp75 antibody.The in vitro OECs of canine grew better than that in man's in the present conditions.Conclusion The method of different attachment time seems available in purifying olfactory ensheathing cells from both the adult canine and man olfactory epithelium.

Mechanisms underlying tolerance to and dependence on anticonvulsant effect of clonazepam are not clear. With in situ hybridization we found CRH mRNA expression increased significantly at paraventricular hypothalamic nucleus in amygdala-kindled rats which had developed tolerance to the anticonvulsant effect of clonazepam, and on day 7 of clonazepam discontinuation CRH mRNA expression no longer changed. Results indicated that CRH was involved in the development of tolerance to and dependence on the anticonvulsant effect of clonazepam.

Combining the observation of rat behavior with the [3H] muscimol radioligand binding experiment, the mechanisms of CZP-antiepileptic effect and tolerance were studied. The audiogenic seizure rats were used, and divided into vehicle control, short time CZP-pretreated, and long time CZP-pretreated group. The results showed that (1) the bell-stimulation made control rats convulse, (2) short time-CZP pretreated rats showed no response to bell; (3) long time-CZP pretreated rats resembled with the control rats; (4) in the short time-CZP pretreated groups, the B(max) binding to GABA(A)-receptor were higher than in the control groups significantly, but the B(max) binding to GABA(A)-receptor did not show significant differences between the control and long-time-CZP pretreated group. The results suggested that CZP inhibited the convulsion of audiogenic seizure rats significantly, and raised the B(max) to GABA(A)-receptor. But long time CZP group lost the antiepileptic effects and the B(max) binding to GABA(A)-receptor were diminished markedly.