The efficacy of cognitive behavioral therapies for depression in China in comparison with the rest of the world: A systematic review and meta-analysis.

OBJECTIVE: There is consistent evidence that cognitive behavioral therapies (CBTs) are effective interventions for adult depression. While some evidence has compared these effects in different countries, no prior systematic review and meta-analysis has compared the efficacy of CBTs between Chinese and people from the rest of the world. The current meta-analysis addressed this gap by a systematic review of eligible studies from Chinese and worldwide databases. METHOD: Hedges' g was calculated using a random-effects model. Subgroup analyses and multilevel meta-analytic models were conducted to examine the relationship among effect sizes and the characteristics in Chinese studies. Metaregression analyses were conducted to explore the difference of the efficacy of CBTs between Chinese studies and non-Chinese studies after controlling for the moderators. RESULTS: A total of 34 (n = 3,710) studies in China and 307 (n = 30,333) studies from the rest of the world were included. The effect size of CBTs on depression for Chinese participants was 1.19 (95% CI [0.86, 1.52]), which was higher (Q = 4.63, p = .03) than the effect size of the rest of the world (0.82, 95% CI [0.74, 0.90]). After controlling for moderators, the effect size of Chinese studies was still higher than non-Chinese studies (ß = 0.351, p = .011). CONCLUSIONS: CBTs are effective interventions for adult depression and deserve more attention in China for depression management. Moderators related to study design, clinical features, and cultural factors need to be considered in the interpretation of the results. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

GDF15 is a major determinant of ketogenic diet-induced weight loss.

A ketogenic diet (KD) has been promoted as an obesity management diet, yet its underlying mechanism remains elusive. Here we show that KD reduces energy intake and body weight in humans, pigs, and mice, accompanied by elevated circulating growth differentiation factor 15 (GDF15). In GDF15- or its receptor GFRAL-deficient mice, these effects of KD disappeared, demonstrating an essential role of GDF15-GFRAL signaling in KD-mediated weight loss. Gdf15 mRNA level increases in hepatocytes upon KD feeding, and knockdown of Gdf15 by AAV8 abrogated the obesity management effect of KD in mice, corroborating a hepatic origin of GDF15 production. We show that KD activates hepatic PPARγ, which directly binds to the regulatory region of Gdf15, increasing its transcription and production. Hepatic Pparγ-knockout mice show low levels of plasma GDF15 and significantly diminished obesity management effects of KD, which could be restored by either hepatic Gdf15 overexpression or recombinant GDF15 administration. Collectively, our study reveals a previously unexplored GDF15-dependent mechanism underlying KD-mediated obesity management.

Effects of starch nanospheres solution on hemodynamic values in rats with hemorrhagic shock: a preliminary study in hemorrhagic shock resuscitation.

BACKGROUND: The objective of the present study was to explore the resuscitation effects of starch nanospheres solution on hemodynamics in rats with hemorrhagic shock. METHODS: A total of 20 Sprague-Dawley rats were randomly divided into 2 groups: resuscitation group 1 (infusion with Ringer's solution) and resuscitation group 2 (infusion with starch nanospheres solution) with 10 rats per group. The rats in resuscitation groups 1 and 2 were subjected to hemorrhagic shock, and resuscitation was performed with Ringer's solution and starch nanospheres solution. The changes in the hemodynamic values of the rats in both groups were observed and recorded. RESULTS: The hemodynamic values included the systolic blood pressure, diastolic blood pressure, mean arterial blood pressure, heart rate, and respiratory rate. After resuscitation, the systolic blood pressure, diastolic blood pressure, mean arterial pressure, and heart rate in resuscitation group 2 had reverted back to the base values (P > 0.05). The systolic blood pressure, diastolic blood pressure, and mean arterial pressure were lower at all points in resuscitation group 1 than in resuscitation group 2 (P < 0.05). The respiratory rate was more rapid after resuscitation at 30 and 60 min in resuscitation group 1 than in resuscitation group 2 (P < 0.05). CONCLUSIONS: Starch nanospheres solution expands the circulating blood volume and improves the hemodynamics. It also increases the effective circulating blood volume and improves the shock symptoms of effective hypovolemia.

Intrinsic and extrinsic effects of mafG deficiency on hematopoietic recovery following bone marrow transplant.

OBJECTIVE: MafG is the small subunit of the transcription factor NF-E2 that controls terminal megakaryocyte maturation and platelet release. Studies were conducted to evaluate the intrinsic and extrinsic effects of mafG deficiency on bone marrow engraftment kinetics. MATERIALS AND METHODS: We used mafG knockout mice either as donors or recipients in bone marrow transplantations with wild-type mice and compared the engraftment kinetics to transplantations using wild-type donors and recipients. We measured peripheral cell counts, the presence of circulating donor-derived cells by flow cytometry, changes in the cellularity of the bone marrow and splenic weight on day 5, 7, 14, and 1 month post-transplantation. RESULTS: Compared to wild-type recipients, mafG recipients had delayed platelet and leukocyte recovery and lower spleen weight at early time points after transplantation. Intrinsic effects: When mafG-deficient bone marrow served as donor source, we observed more rapid recovery of bone marrow cellularity and increased splenic hematopoiesis. The finding of increased short-term hematopoietic stem cells and progenitors in the mafG-deficient bone marrow could explain the accelerated hematopoietic recovery after transplantation. Furthermore, the expression of Bach 2, which can form a heterodimer with mafG protein, was found to be greatly reduced, while Notch 1 expression was increased in mafG-deficient mice. Extrinsic effects: When mafG-deficient mice were transplant recipients, there were delays in recovery of normal levels of marrow and splenic hematopoiesis as well as circulating leukocytes and platelets. CONCLUSIONS: Our study demonstrates that mafG expression has intrinsic and extrinsic effects on hematopoietic engraftment following bone marrow transplantation.

[Study on the relationship among lifestyle, self-esteem and life satisfaction in Chinese adolescents].

OBJECTIVE: To explore the relationship between lifestyle, self-esteem and life satisfaction among Chinese adolescents. METHODS: 10 899 adolescents in middle schools and colleges from 9 provinces in China were investigated by using Chinese Adolescent Lifestyle Scale (CALS), Rosenberg Self-Esteem Scale (SES). RESULTS: The distribution of adolescents in the four groups divided by lifestyle and life satisfaction scores were different regarding the area and grade of these students(chi(2)=248.93, P<0.01;chi(2)=568.53, P<0.01). A high percentage of adolescents in cities (58.9%) reported a healthy life style with high life satisfaction while most adolescents in rural areas (58.9%) reported poor life styles with little satisfaction. A high percentage of junior high school students (61.8%) reported a healthy life style with high life satisfaction, but this percentage among senior high school and college students was down to 48.5% and 21.3% respectively. About 7.6% of senior high school students reported a healthy life style but poor satisfaction, a little higher than that of junior high school students (4.1%) and college students (3.6%). Moreover, there were 71.6% college students reported that they lead a poor life style with little satisfaction. The lifestyle is significantly correlated with self-esteem (r=0.472, P<0.01) and life satisfaction(r=0.636, P<0.01), and self-esteem is also significantly correlated with life satisfaction (r=0.450, P<0.01). self-esteem was the mediator of the other two parameters. CONCLUSION: The lifestyle predicts life satisfaction through self-esteem. Area and grade differences have to be taken into consideration when introducing programs on health promotion, and attention should be attached to the influence of psychological factors.

[Association of urinary albumin excretion rate and hyperuricemia with macrovascular atherosclerosis in type 2 diabetic patients].

OBJECTIVE: To investigate the association of urinary albumin excretion rate (UAER) and hyperuricemia with macrovascular atherosclerosis in type 2 diabetic patients. METHODS: Ninety-seven type 2 diabetic patients were divided into two groups according to the UAER, namely group A with UAER between 20 and 200 microg/min (n=63) and group B with UAER > or = 200 microg/min (n=34); the patients were also classified into hyperuricemia group (group C, n=59) and normal blood uric acid (BUA) group (group D, n=38). The disease course, BUA, fasting blood glucose (FBG), triglyceride (TG), total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoproteins (HDL), UAER and arteria carotis intima-media thickness (IMT) were determined in these patients. The relationship of UAER and hyperuricemia with carotid arterial IMT was analyzed statistically. RESULTS: The levels of TG, TC, LDL and HDL showed no significant differences between the 4 groups (P>0.05). The disease course, BUA, UAER, and FBG levels and IMT in groups A and C were significantly higher than those in groups C and D (P<0.05), but no such differences were found between groups A and C or between groups B and D (P>0.05). Arotid arterial IMT was independently correlated to the disease course, BUA and UAER (r=0.201, 0.1999, 0.211, respectively, P<0.05), and a significant positive correlation was noted between BUA and UAER (r=0.221, P<0.05). CONCLUSION: Macrovascular atherosclerosis in type 2 diabetic patients is significantly correlated to the disease course, BUA and UAER levels, which can be used to evaluate and predict macrovascular atherosclerosis in type 2 diabetic patients.

High levels of acetylated low-density lipoprotein uptake and low tyrosine kinase with immunoglobulin and epidermal growth factor homology domains-2 (Tie2) promoter activity distinguish sinusoids from other vessel types in murine bone marrow.

BACKGROUND: The bone marrow contains a variety of blood vessels that have different functions in bone marrow maintenance and hematopoiesis. Arterioles control the flow of blood into bone marrow compartments, and sinusoids serve as a conduit to the bloodstream and as niches for megakaryocyte development. Most studies of bone marrow vasculature, including studies quantifying changes in the marrow vascular by microvascular density, do not differentiate between different types of marrow vessels. Recognizing changes in different types of blood vessels after chemotherapy exposure or during leukemia development has important physiological implications. We hypothesized that the functional heterogeneity of marrow vasculature could be recognized through the use of functional markers such as tyrosine kinase with immunoglobulin and epidermal growth factor homology domains-2 (Tie2) expression or 1,1-dioctadecyl -3,3,3,3-tetramethyl-indocarbocyanine perchlorate with acetylated low-density lipoprotein (DiI-Ac-LDL) uptake. METHODS AND RESULTS: When transgenic mice with green fluorescent protein (GFP) expressed downstream of the Tie2 promoter were injected with Ac-LDL, Ac-LDL was specifically endocytosed by sinusoids, and Tie2 expression was more pronounced in the arteries, arterioles, and transitional capillaries. Combining these 2 functional endothelial markers and using confocal microscopy to obtain 3-dimensional images, we identified transitional zones where arterioles emptied into the sinusoids. Alternatively, coinjection of lectin with DiI-Ac-LDL has a similar result in normal mice, as seen in Tie2/GFP mice, and can be used to differentiate vessel types in nontransgenic mice. CONCLUSIONS: These results demonstrate that bone marrow vasculature is functionally heterogeneous. Methods to study changes in the marrow vasculature using microvascular density or quantifying changes in the vascular niche need to take this heterogeneity into account.

Bone marrow sinusoidal endothelial cells undergo nonapoptotic cell death and are replaced by proliferating sinusoidal cells in situ to maintain the vascular niche following lethal irradiation.

OBJECTIVE: Bone marrow sinusoids remain predominantly host-derived following bone marrow transplantation. Systematic analysis was conducted at the cellular level to investigate how the host sinusoidal structures survived after lethal irradiation. MATERIALS AND METHODS: Apoptosis and cell proliferation assays were performed on bone marrow sections at various time points during the first 2 weeks postirradiation to study the extent of damage to sinusoidal endothelial cells from lethal irradiation and to determine whether cell proliferation contributes to the recovery of the sinusoidal system. RESULTS: Phosphorylated H2AX was present in both hematopoietic and sinusoidal endothelial cells 3 hours after irradiation demonstrating DNA damage. Three days after irradiation, some sinusoidal endothelial cells became terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling -positive, but were caspase-3 and in situ oligo ligation -negative, suggesting nonapoptotic DNA fragmentation. Clusters of sinusoidal endothelial cells that expressed Ki67 appeared 3 days after irradiation, and increased through day 7. These Ki67-positive endothelial cells were host-derived. Bromodeoxyuridine-positive endothelial cells were present in the Ki67-positive areas confirming endothelial cell replication. Twenty percent of the sinusoidal endothelial cells were lost by day 3 after irradiation. The total number of endothelial cells remained relatively unchanged between day 3 and day 14. These results demonstrate that lethal irradiation resulted in limited, nonapoptotic sinusoidal endothelial cell loss, followed by proliferation of preexisting host-derived mature sinusoidal endothelial cells. Our data suggest that DNA repair mechanisms and proliferation of host endothelial cells within the sinusoids are involved in maintenance of the structural integrity of the bone marrow vascular niche following lethal irradiation.

Sites and kinetics of donor thrombopoiesis following transplantation of whole bone marrow and progenitor subsets.

INTRODUCTION: Little is known about the sites and kinetics of thrombopoiesis following bone marrow transplant. The spleen is a site of hematopoiesis in a healthy mouse, and hematopoietic activity increases in response to stress. We hypothesized that the spleen is a major site of early post-transplant thrombopoiesis. METHODS: We transplanted whole bone marrow (WBM) or lineage depleted progenitor subsets fractionated based on expression of c-kit and Sca-1 from transgenic mice expressing green fluorescent protein into lethally irradiated C57BL/6 recipients. We also transplanted whole bone marrow cells into healthy and splenectomized mice. Post-transplant megakaryopoiesis was assessed by measuring circulating platelet number, percent donor-derived platelets, bone marrow cellularity, splenic weight, megakaryocyte size, and megakaryocyte concentration from hour 3 to day 28 post transplant. RESULTS: Following transplant, circulating donor-derived platelets were derived only from c-kit expressing subsets. Donor-derived platelets first appeared on post-transplant day five. Splenectomy reduced the number of these earliest circulating platelets. Splenic megakaryopoiesis increased dramatically from day 7-14 post-transplant. However, splenectomy accelerated platelet engraftment during this time frame. CONCLUSION: Overall, these results demonstrate that the first platelets are produced by c-kit expressing megakaryocyte progenitors in the bone marrow and spleen. After post-transplant day 5, the net effect of the spleen on thrombopoiesis is to slow engraftment due to immune effects or hypersplenism.

The role of the donor in the repair of the marrow vascular niche following hematopoietic stem cell transplant.

Bone marrow sinusoids maintain homeostasis between developing hematopoietic cells and the circulation, and they provide niches for hematopoietic progenitors. Sinusoids are damaged by chemotherapy and radiation. Hematopoietic stem cells (HSCs) have been shown to produce endothelial progenitor cells that contribute to the repair of damaged blood vessels. Because HSCs home to the marrow during bone marrow transplant, these cells may play a role in repair of marrow sinusoids. Here, we explore the role of donor HSCs in the repair of damaged sinusoids following hematopoietic stem cell transplant. We used three methods to test this role: (a) expression of platelet endothelial cell adhesion molecule to identify endothelial progenitors and the presence of the Y chromosome to identify male donor cells in female recipients; (b) presence of the Y chromosome to identify male donor cells in female recipients, and expression of the panendothelial marker mouse endothelial cell antigen-32 to identify sinusoidal endothelium; and (c) use of Tie-2/green fluorescent protein mice as donors or recipients and presence of Dil-Ac-LDL to identify sinusoids. We found that sinusoids were predominantly host-derived posttransplant. Donor cells spread along the marrow vasculature early post-transplant in a pattern that matched stromal-derived factor-1 expression. Furthermore, these engrafting progenitors were positioned to provide physical support, as well as growth and survival signals in the form of vascular-endothelial growth factor-A. Occasionally, donor cells provide cellular "patches" in the damaged sinusoids, although this occurred at a low level compared with hematopoietic engraftment. Donor support for the repair of the marrow vascular niche may be a critical first step of hematopoietic engraftment.

Umbilical cord blood produces small megakaryocytes after transplantation.

Delayed platelet engraftment is a major complication of umbilical cord blood (CB) transplantation. Megakaryocytes derived from CB in vitro are smaller than megakaryocytes derived from bone marrow (BM) or mobilized peripheral blood from adults. Small megakaryocyte size may contribute to delayed platelet engraftment. To test whether small size persists after transplantation, we measured megakaryocyte size, concentration, and maturational stage in BM biopsy specimens obtained after transplantation in archived BM samples from patients receiving CB (CB group, n = 10) versus mobilized peripheral blood or BM transplantation (BM group, n = 9). Megakaryocytes in the postengraftment BM samples were significantly smaller in the CB group than in the BM group (median diameter, 16.7 vs 22.0 microm). There were no significant differences in megakaryocyte concentration or maturational stage between the CB and BM groups. For the first time, we demonstrate that the attainment of adult size in CB-derived megakaryocytes is delayed after human CB transplantation.

Developmental differences in megakaryocyte maturation are determined by the microenvironment.

Historically, physicians have attributed delayed platelet engraftment following umbilical cord blood transplant to decreased numbers of stem cells in cord blood compared with adult bone marrow. However, recent studies suggest that delayed platelet engraftment may be caused by an intrinsic inability of neonatal stem cells to produce mature, polyploid megakaryocytes. We tested this hypothesis by transplanting adult bone marrow and newborn liver hematopoietic stem and progenitor cells from transgenic mice expressing green fluorescent protein into myeloablated wild-type recipients and comparing the size and ploidy levels of megakaryocytes that developed in adult transplant recipients. Transplanted stem and progenitor cells, regardless of their source, gave rise to megakaryocytes that were larger than normal adult megakaryocytes as early as 7 days post-transplant. However, megakaryocytes that developed after transplant of neonatal stem and progenitor cells were significantly smaller than those derived from adult stem and progenitor cells. Furthermore, megakaryocytes derived from neonatal cells had lower ploidy values than megakaryocytes derived from adult cells at 18 days post-transplant, when ploidy could first be reliably measured in the bone marrow. These differences in size and ploidy disappeared by 1 month post-transplant. The largest megakaryocytes developed in the spleen. These results suggest that, in the mouse, the microenvironment is responsible for some of the maturational differences in size and ploidy between neonatal and adult megakaryocytes. Furthermore, neonatal and adult megakaryocyte progenitors also have cell-intrinsic differences in the way they engraft and respond to thrombocytopenic stress. These differences may contribute to the delay in platelet engraftment that frequently complicates cord blood transplants.