Objective To investigate the effects of ginkgolide B on neuronal cell apoptosis,superoxide dismutase activity,malondialdehyde,interleukin-1beta,tumor necrosis factor-alpha,and interleukin-6 levels in serum of rats with intracerebral hemorrhage in order to explore the role of ginkgolide B in suppressing the neuronal cell apoptosis.Methods A total of 175 male Wistar rats were randomly (random number)divided into sham operation group,intracerebral hemorrhage group,as well as low,medium and high dose treatment groups.The rat model of intracerebral hemorrhage was made with infusion of autologous whole blood to caudate nucleus in the right basal ganglia region.Ginkgolide B in dose of 5 mg/kg,10 mg/kg and 20 mg/kg was given to rats in the low,middle and high dose treatment groups by intraperitoneal injection once a day for 5 days after intracerebral hemorrhage.The rats with intracerebral hemorrhage in the sham operation groups received intraperitoneal administration of 1 mL saline.Animals were sacrificed by decapitation 2,6,12,24,48,72 h and 5 days after intracerebral hemorrhage.Brains were taken and blood samples were collected.Neuronal cell apoptosis was measured by using terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling(TUNEL),and superoxide dismutase activity in serum was determined by using xanthine oxidase method,and serum malondialdehyde level was detected by using thiobarbituric acid reactive substance assay,and interleukin-1beta,tumor necrosis factor-alpha,and interleukin-6 levels in serum were assayed with enzyme linked immunosorbent assay(ELISA).Statistical analysis was carried out by using one-way analysis of variance and least-significant difference test.Results As 2 h,6 h,12 h,24 h,48 h,72 h,and 5 days after intracerebral hemorrhage,the differences in the number of apoptotic neuronal cell,superoxide dismutase activity in serum,serum malondialdehyde,interleukin-1 beta,tumor necrosis factor-alpha and interleukin-6 levels between the low dose treatment group and intracerebral hemorrhage group were not significant statistically(P ＞0.05).As 12 h,24 h,72 h,and 5 days after intracerebral hemorrhage,the number of apoptotic neuronal cell,superoxide dismutase activity in serum,serum malondialdehyde,interleukin-1 beta,tumor necrosis factor-alpha and interleukin-6 levels in the medium dose and high dose treatment groups were significantly statistically lower than those in the intracerebral hemorrhage group(P ＜ 0.05),but these differences in above biomarkers were not significant statistically among these three groups 2 and 6 hours after intracerebral hemorrhage(P ＞ 0.05).Conclusions Ginkgolide B may lessen neuronal cell apoptosis by means of inhibition of free radical production and inflammatory reactions after intracerebral hemorrhage.

Objective To explore the effect of insulin subcutaneous pump combined with psychological intervention on gestational diabetes mellitus.Methods A total of 118 patients were enrolled in this study from November 2015 to October 2016 in Lishui central hospital.The patients were randomly divided into the experimental group and the control group according to the time of hospitalization.The experimental group was given insulin subcutaneous pump combined with psychological intervention.The control group was given insulin subcutaneous pump.Results After intervention, the degree of complete compliance in the experimental group was 86.44% and 28.81% before intervention, the difference was statistically significant(P<0.05).Compared with before treatment, blood glucose and glycosylated hemoglobin were decreased after treatment(P<0.05).The incidence of complications in the two groups include: pregnant women with excessive amniotic, neonatal hypoglycemia, pregnancy induced hypertension syndrome and so on.The difference of complication rate between the two groups was statistically significant(P<0.05).Conclusion The timely and accurate psychological guidance of pregnant women with diabetes mellitus can control the blood glucose in the normal range, reduce the occurrence and development of maternal and child complications, and ensure the safe and healthy mother and child health.

Tooth number abnormality is one of the most common dental developmental diseases, which includes both tooth agenesis and supernumerary teeth. Tooth development is regulated by numerous developmental signals, such as the well-known Wnt, BMP, FGF, Shh and Eda pathways, which mediate the ongoing complex interactions between epithelium and mesenchyme. Abnormal expression of these crutial signalling during this process may eventually lead to the development of anomalies in tooth number; however, the underlying mechanisms remain elusive. In this review, we summarized the major process of tooth development, the latest progress of mechanism studies and newly reported clinical investigations of tooth number abnormality. In addition, potential treatment approaches for tooth number abnormality based on developmental biology are also discussed. This review not only provides a reference for the diagnosis and treatment of tooth number abnormality in clinical practice but also facilitates the translation of basic research to the clinical application.
Gene Expression Regulation, Developmental ; Odontogenesis ; Signal Transduction ; Tooth/metabolism* ; Humans

Neural crest-derived mesenchymal stem cells (MSCs) are known to play an essential function during tooth and skeletal development. PRX1⁺ cells constitute an important MSC subtype that is implicated in osteogenesis. However, their potential function in tooth development and regeneration remains elusive. In the present study, we first assessed the cell fate of PRX1⁺ cells during molar development and periodontal ligament (PDL) formation in mice. Furthermore, single-cell RNA sequencing analysis was performed to study the distribution of PRX1⁺ cells in PDL cells. The behavior of PRX1⁺ cells during PDL reconstruction was investigated using an allogeneic transplanted tooth model. Although PRX1⁺ cells are spatial specific and can differentiate into almost all types of mesenchymal cells in first molars, their distribution in third molars is highly limited. The PDL formation is associated with a high number of PRX1⁺ cells; during transplanted teeth PDL reconstruction, PRX1⁺ cells from the recipient alveolar bone participate in angiogenesis as pericytes. Overall, PRX1⁺ cells are a key subtype of dental MSCs involved in the formation of mouse molar and PDL and participate in angiogenesis as pericytes during PDL reconstruction after tooth transplantation.
Animals ; Cell Differentiation ; Mesenchymal Stem Cells ; Mice ; Molar ; Osteogenesis/physiology* ; Periodontal Ligament

In growing children, growth plate cartilage has limited self-repair ability upon fracture injury always leading to limb growth arrest. Interestingly, one type of fracture injuries within the growth plate achieve amazing self-healing, however, the mechanism is unclear. Using this type of fracture mouse model, we discovered the activation of Hedgehog (Hh) signaling in the injured growth plate, which could activate chondrocytes in growth plate and promote cartilage repair. Primary cilia are the central transduction mediator of Hh signaling. Notably, ciliary Hh-Smo-Gli signaling pathways were enriched in the growth plate during development. Moreover, chondrocytes in resting and proliferating zone were dynamically ciliated during growth plate repair. Furthermore, conditional deletion of the ciliary core gene Ift140 in cartilage disrupted cilia-mediated Hh signaling in growth plate. More importantly, activating ciliary Hh signaling by Smoothened agonist (SAG) significantly accelerated growth plate repair after injury. In sum, primary cilia mediate Hh signaling induced the activation of stem/progenitor chondrocytes and growth plate repair after fracture injury.
Mice ; Animals ; Hedgehog Proteins/genetics* ; Receptors, G-Protein-Coupled/metabolism* ; Cilia/metabolism* ; Cartilage/metabolism* ; Regeneration