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Adipokine Apelin/APJ Walkway Encourages Peritoneal Dissemination of Ovarian Cancers Cells by Regulatory Fat Fat burning capacity.
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Light is a salient cue that can influence neurodevelopment and the immune system. Light exposure out of sync with the endogenous clock causes circadian disruption and chronic disease. Nintedanib Environmental light exposure may contribute to developmental programming of metabolic and neurological systems but has been largely overlooked in Developmental Origins of Health and Disease (DOHaD) research. Here, we investigated whether developmental light exposure altered programming of visual and metabolic systems.

Pregnant mice and pups were exposed to control light (1212 lightdark) or weekly light cycle inversions (circadian disruption [CD]) until weaning, after which male and female offspring were housed in control light and longitudinally measured to evaluate differences in growth (weight), glucose tolerance, visual function (optomotor response), and retinal function (electroretinogram), with and without high fat diet (HFD) challenge. Retinal microglia and macrophages were quantified by positive Iba1 and CD11b immunofluorescence.

CD exposure caused impaired visual function and increased retinal immune cell expression in adult offspring. When challenged with HFD, CD offspring also exhibited altered retinal function and sex-specific impairments in glucose tolerance.

Overall, these findings suggest that the light environment contributes to developmental programming of the metabolic and visual systems, potentially promoting a pro-inflammatory milieu in the retina and increasing the risk of visual disease later in life.
Overall, these findings suggest that the light environment contributes to developmental programming of the metabolic and visual systems, potentially promoting a pro-inflammatory milieu in the retina and increasing the risk of visual disease later in life.
To investigate the association between serum uric acid (SUA) levels and vision-threatening diabetic retinopathy (VTDR) in patients with type 2 diabetes.

This cross-sectional study evaluated 3481 patients with type 2 diabetes from four communities in China between 2016 and 2019. VTDR was defined as severe nonproliferative, proliferative diabetic retinopathy, or clinically significant macular edema evaluated by fundus photography and optical coherence tomography. Potential association between SUA and VTDR was examined using multivariable logistic regression. Sub-group analyses based on sex were constructed.

A total of 305 participants had VTDR. Both higher SUA (odds ratio [OR], 1.22 per 100 µmol/L; 95% confidence interval [CI], 1.04-1.44; P = 0.013) and hyperuricemia (OR, 1.47; 95% CI, 1.07-2.04; P = 0.019) were positively associated with VTDR after adjustment for relevant covariates. Compared with those in the lowest SUA quartile, participants in the third (OR, 1.60; 95% CI, 1.07-2.39; P = 0.022) and fourth (OR, 2.05; 95% CI, 1.37-3.08; P = 0.001) sex-specific SUA quartiles showed a significantly increased risk of VTDR after adjustment. No sex-related difference was observed.

Higher SUA levels were associated with an increased risk of VTDR in patients with type 2 diabetes in both sexes, although females seemed to be more sensitive to high SUA than males. Prospective cohort studies are needed to verify SUA as a biomarker for predicting the risk of VTDR. Whether decreased SUA levels could decrease the risk of VTDR also requires further investigation.
Higher SUA levels were associated with an increased risk of VTDR in patients with type 2 diabetes in both sexes, although females seemed to be more sensitive to high SUA than males. Prospective cohort studies are needed to verify SUA as a biomarker for predicting the risk of VTDR. Whether decreased SUA levels could decrease the risk of VTDR also requires further investigation.Lipid droplets (LDs) are critical for lipid storage and energy metabolism. LDs form in the endoplasmic reticulum (ER). However, the molecular basis for LD biogenesis remains elusive. Here, we show that fat storage-inducing transmembrane protein 2 (FIT2) interacts with ER tubule-forming proteins Rtn4 and REEP5. The association is mainly transmembrane domain based and stimulated by oleic acid. Depletion of ER tubule-forming proteins decreases the number and size of LDs in cells and Caenorhabditis elegans, mimicking loss of FIT2. Through cytosolic loops, FIT2 binds to cytoskeletal protein septin 7, an interaction that is also required for normal LD biogenesis. Depletion of ER tubule-forming proteins or septins delays nascent LD formation. In addition, FIT2-interacting proteins are up-regulated during adipocyte differentiation, and ER tubule-forming proteins, septin 7, and FIT2 are transiently enriched at LD formation sites. Thus, FIT2-mediated nascent LD biogenesis is facilitated by ER tubule-forming proteins and septins.
The inferior petroclival vein (IPV) courses along the extracranial surface of the petroclival fissure. It is occasionally involved in vascular diseases and has recently been used for vascular access to the cavernous sinus. However, detailed descriptions of its anatomy are currently lacking.

To define the anatomic relationship between the IPV and its surrounding structures based on cadaveric dissection and radiological analysis.

A dry skull and an injected cadaver head were examined to reveal the relationships between the IPV and its surrounding structures. The existence of the IPV and its relationships with other venous structures were also examined by contrast-enhanced, fat-suppressed T1-weighted magnetic resonance imaging in 26 patients (51 sides).

The entire course of the IPV was shown via stepwise cadaver dissection from below. Its relationships with surrounding structures, such as the jugular bulb, sigmoid sinus, inferior petrosal sinus, petrosal venous confluence, and the posterior, lateral, and anterior condylar veins, were also shown. In the radiological analysis, the IPV was identified on all sides. The rostral end of the vein was connected to the venous plexus around the carotid artery on all sides. The vein drained into the caudal end of the inferior petrosal sinus (49/51 sides, 96.1%) or into the anterior condylar vein (2/51 sides, 3.9%).

A precise understanding of the anatomy of the IPV will enable endovascular and skull base surgeons to achieve diagnoses and gain safe access to lesions involving the IPV.
A precise understanding of the anatomy of the IPV will enable endovascular and skull base surgeons to achieve diagnoses and gain safe access to lesions involving the IPV.
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