Ultrasonographic abdominal adipose tissue thickness for the prediction of gestational diabetes mellitus: A meta-analysis.

Obesity has been linked to the risk of gestational diabetes mellitus (GDM). The meta-analysis aimed to assess the predictive role of ultrasonographic measurements of the abdominal adipose tissue thickness for GDM in pregnant women. Cohort studies evaluating the association between abdominal subcutaneous and/or visceral adipose thickness (SAT and/or VAT) and subsequent risk of GDM were retrieved from PubMed, Embase, and Web of Science databases. Only studies with SAT/VAT measured before the diagnosis of GDM were included. Random-effects models incorporating the influence of potential heterogeneity were used to pool the results. A total of 13 studies involving 5616 pregnant women were included. Pooled results showed that both a high abdominal SAT (odds ratio [OR] for per 1-cm increment: 1.23, 95% confidence interval [CI]: 1.07 to 1.41, P = 0.003, I2 = 13%; OR for high versus low category: 3.42, 95% CI: 2.31 to 5.07, P < 0.001, I2 = 0%) and VAT (OR for per 1-cm increment: 1.54, 95% CI: 1.16 to 2.06, P = 0.003, I2 = 63%; OR for high versus low category: 5.73, 95% CI: 3.39 to 9.77, P < 0.001, I2 = 31%) at early stages of pregnancy were associated with a higher subsequent risk of GDM. Subgroup analysis based on study design, timing of ultrasound examination, GDM diagnostic criteria, and study quality score showed consistent results. In conclusion, ultrasound-measured abdominal adipose tissue thickness may be useful for predicting the subsequent risk of GDM in pregnant women.

Influence of renal function on the ability of TyG Index to predict all-cause mortality.

BACKGROUND: The association between triglyceride-glucose (TyG) index and poor prognosis remains controversial. Whether renal function status affects the ability of the TyG index to predict poor prognosis has not yet been elucidated and merits further studies. METHODS: This retrospective cohort study included 22,031 participants from communities in the U.S. By juxtaposing the TyG categories with the estimated glomerular filtration rate (eGFR, either < 60 mL/min/1.73m2 or ≥ 60 mL/min/1.73m2), participants were categorized into four distinct groups: (1) TyG_L/eGFR_H; (2) TyG_H/eGFR_H; (3) TyG_L/eGFR_L; and (4) TyG_H/eGFR_L. The endpoint was the all-cause mortality rate. Standard Kaplan-Meier plots were constructed and multifactor Cox regression analyses were carried out and restricted cubic spline regression analysis was utilized to assess the association between death and the TyG index for different renal function statuses. RESULTS: No statistical differences were found in the TyG groups in participants with normal renal function after adjustment for all covariates (P = 0.070). However, in the high TyG index group with renal insufficiency, the risk of all-cause mortality rates was reduced by 18%. (HR, 0.82; CI, 0.69-0.98). The TyG index (high vs. low) and renal function (eGFR < 60 vs. eGFR ≥ 60) had statistically significant interactions with death (P < 0.001). When all covariates were adjusted, the risk of mortality for the TyG_L combined with eGFR_L group was 56% higher than that for the TyG_L combined with eGFR_H group (HR, 1.56; CI, 1.33-1.82). In the renal insufficiency population, a nonlinear relationship was observed between mortality and the TyG index, albeit with a differing pattern (P for nonlinearity < 0.001). CONCLUSIONS: While it has been known that TyG index was a prognosis marker of CVD, this research highlights that higher TyG index was associated with higher all-cause mortality rates for all participants. Furthermore, renal function status significantly moderates the effect of the TyG index on all-cause mortality in community-dwelling adults.

An Exploration of Oral-Gut Pathogens Mediating Immune Escape of Pancreatic Cancer via miR-21/PTEN Axis.

Oral-gut pathogens are closely associated with pancreatic cancer, such as Campylobacter jejuni, Clostridium difficile, Enterococcus faecalis, Escherichia coli, Fusobacterium nucleatum, Helicobacter pylori, Porphyromonas gingivalis, and Vibrio cholera, but the related mechanisms remain not well understood. Phosphatase and tensin homolog (PTEN, a widely known tumor suppressor) play a key role in the anti-cancer immune system. Pancreatic cancer cells with PTEN loss are often in the immunosuppressive tumor microenvironment regulated by myeloid-derived suppressor cells (MDSCs), regulatory T cells (Tregs), and M2 macrophages, which are regarded as the mechanism in the immune escape of cancers. The miR-21, as an oncogene in human cancers, plays an important role in pancreatic cancer progression, downregulates the levels of PTEN, and may promote cancer to evade host immune surveillance. Some oral-gut pathogens have been found to promote miR-21 expression and reduce PTEN expression. On the other hand, most gut pathogens infection is thought to produce reactive oxygen species (ROS) or activate inflammatory cytokines, which may also induce ROS-mediated miR-21 expression. These pathogens' infection is involved with the cell density of MDSCs, Tregs, and M2 macrophages. Therefore, it is quite reasonable to propose that oral-gut pathogens possibly promote pancreatic cancer escaping from host immune surveillance by activating the miR-21/PTEN axis and immune-suppressive cells. The present exploration suggests that an increased understanding of the pattern of the effects of gut pathogens on the miR-21/PTEN axis will lead to better insights into the specific mechanisms associated with the immune escape of pancreatic cancer caused by oral-gut microbiota.

The mitochondrial genome and phylogenetic position of a conehead katydid Euconocephalus pallidus (Insecta: Orthoptera).

The complete mitochondrial genome of a conehead katydid Euconocephalus pallidus was determined. The mitochondrial genome is 15,888 bp in size with an A + T content of 71.67%. It contains 13 protein-coding genes, 22 transfer RNA genes, two ribosomal RNA genes, and a control region. The order and orientation of these genes conform to the ancestral form of insects. Phylogenetic analysis supports a close relationship between E. pallidus and E. nasutus.

Effects of alteplase on neurological deficits and expression of GFAP and GAP-43 in brain tissue of rats with acute cerebral infarction.

OBJECTIVE: To investigate the effects of alteplase on neurological deficits, as well as on the expressions of glial fibrillary acidic protein (GFAP) and growth-associated protein-43 (GAP-43) in brain tissues of rats with acute cerebral infarction (ACI). METHODS: Sprague Dawley (SD) rats (n = 50) were enrolled in a trial to establish a ACI rat model; of these, 48 rats were succeeefully modeled and were randomized into either the model or alteplase group, whereas another 24 SD rats were included in the sham-operated group. FINDINGS: No significant difference in scores was observed between the model and alteplase groups at T1 (P > 0.05); however, rats in the alteplase group demonstrated lower scores than those in the model group at T2, T3, and T4 (P < 0.05). Rats in the model group showed a larger cerebral infarction volume than those in the alteplase group (P < 0.05), and the infarction volume on day 1, 3, 6, and 9 was higher in rats in the alteplase group than those in the sham-operated group (P < 0.05). CONCLUSION: Treatment with alteplase can be effective in reducing cerebral infarction volume and moderating neurological deficits in ACI modeled rats within a 6-h time window, which may be correlated with the regulation of GFAP and GAP-43 expressions by alteplase.

Effect of transplanted mesenchymal stem cells from rats of different ages on the improvement of heart function after acute myocardial infarction.

BACKGROUND: Mesenchymal stem cells (MSCs) transplantation is of therapeutic potential after ischemic injury in both experimental and clinical studies. Clinically, elderly patients are more vulnerable to acute myocardial infarction (AMI). But little is known about the characteristics of young donor-derived MSCs transplanted to old patients with AMI. The present study was designed to investigate the effect of transplanted MSCs from rats of different ages on the improvement of heart function after AMI. METHODS: MSCs from Sprague-Dawley (SD) rats were isolated and cultured in vitro. The apoptosis characteristics of MSCs were observed under conditions of ischemia and anoxia. SD rats underwent MI received intramyocardial injection of MSCs from young donor rats (n = 8), old donor rats (n = 8), respectively. AMI control group received equal volume physiological saline. Immunofluorescence was used to observe the differentiation of the grafted cells into cardiomyocytes. Four weeks after cell transplantation, reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry for vascular endothelial growth factor (VEGF), VIII-factor immunohistochemistry for vessel density, TUNEL, caspase-3 for cardiomyocyte apoptosis, echocardiography and hemodynamic detection for heart function were performed. RESULTS: The apoptosis rate of the old donor-derived MSCs group was significantly higher than that of the young donor-derived MSCs group under conditions of ischemia and anoxia (P < 0.05). Engrafted MSCs survived, proliferated and differentiated into myocardium-like cells. VEGF gene expression and capillary density in the old donor-derived group were lower than those in the young donor-derived group but higher than those in the control group (P < 0.05). The transplantation of old donor-derived MSCs attenuated apoptosis of cardiomyocytes in the peri-infarct region compared with the control group and the effect was elevated in young donor-derived MSCs (P < 0.05). The heart functions (left ventricle ejection fraction (LVEF), left ventricle fractional shortening (LVFS)) were improved more significantly in the old donor-derived MSCs group than in the control group and the heart function in the young donor-derived MSCs group further improved (P < 0.05). CONCLUSIONS: Young donor-derived MSCs can improve heart function significantly through angiogenesis and decreasing cardiomyocyte apoptosis when transplanted to the infarcted area.