The development and functioning of the human fetoplacental vascular system are vulnerable to the maternal diabetic milieu. These vessels are in direct continuum with the fetal vascular system and are therefore also vulnerable to fetal endocrine derangements. Increased angiogenesis, altered junctional maturity and molecular occupancy, together with increased leakiness, constitute a well-described phenotype of vessels in the Type 1 diabetic human placenta and can be related to increased levels of placental vascular endothelial growth factor. The causes of these observed changes, whether maternal hyperglycaemia or fetal hyperinsulinaemia, still remain to be shown in the human placenta. Mechanistic studies using different vascular systems have shown high glucose and insulin to have profound vascular effects, with elevations in vascular endothelial growth factor, nitric oxide and protein kinase C being behind alterations in junctional adhesion molecules such as occludin and vascular endothelial-cadherin and vascular leakage of albumin. The role of advanced glycation products and oxidative stress in this vascular pathology is also discussed. The altered molecular mechanisms underlying the vascular changes in the diabetic human placenta may reflect similar consequences of high glucose and hyperinsulinaemia.

Vascular dysfunction in the diabetic placenta: causes and consequences.

ObjectivesTo explore the risk of development of sudden sensorineural hearing loss (SSHL) among diabetes mellitus patients.Study DesignA retrospective cohort study.SettingPopulation-based study of Taiwan National Health Insurance Research Database.PatientsApproximately 26,556 newly diagnosed diabetic

Risk of developing sudden sensorineural hearing loss in diabetic patients: A population-based cohort study

Objectives/Hypothesis:

To examine the risk of getting Sudden Sensorineural Hearing Loss (SSHL) among patients with chronic kidney disease (CKD).



Study Design:

A retrospective cohort study.



Methods:

Population-based representative insurance claims data were used to examine the risk of getting SSHL among patients with chronic kidney disease. Data extracted from the Taiwan National Health Insurance Research Database yielded 37,421 patients with newly diagnosed renal insufficiency and 37,421 subjects without renal insufficiency from between 2000 and 2004.



Results:

The incidence of SSHL at the end of 2009 was determined. The incidence of SSHL was 1.57 times higher in the CKD-carrying group compared to the incidence in the non-CKD group (10.24 vs. 6.52 per 10,000 person-years), with adjusted hazard ratio (HR) of 1.46 (95% CI = 1.194–1.787) using Cox proportional hazard regressions. Age was an independent risk factor of getting SSHL, with adjusted HRs of 2.01, 3.178, and 2.285 for age ranges of 35 ≈ 49, 50 ≈ 64 and ≥ 65 compared with age range of 0 ≈ 35. Diabetes Mellitus was another independent risk factor with HR of 1.31 (95% CI = 1.003–1.711).



Conclusions:

Present results suggested a significant association between CKD and increased risk of getting SSHL. Comorbidity of diabetes in patients with CKD appeared to be associated with increased risk of getting SSHL, especially for the patients who are 35 years of age and older. Laryngoscope, 2013

Increased risk of getting sudden sensorineural hearing loss in patients with chronic kidney disease: a population-based cohort study.

Sudden sensorineural hearing loss (SSHL) is a clinically common acute symptom in otolaryngology. Although the incidence of SSHL has increased around the world in recent years, the etiology of the disease is still unclear. It has been reported that infections, ototoxic drugs, membrane labyrinth rupture, carcinomas, circulatory system diseases, autoimmune diseases, brain lesions, mental diseases, congenital or inherited diseases, and so on, are all risk factors for SSHL. Here, we discuss the autoimmune mechanisms behind SSHL, which might be induced by type II–IV allergic reactions. We also introduce the main immunosuppressive medications that have been used to treat SSHL, which will help us to identify potential targets for immune therapy.

/pdf/the-role-of-autoimmunity-in-the-pathogenesis-of-sudden-2dmtyssa5b.pdf

The Role of Autoimmunity in the Pathogenesis of Sudden Sensorineural Hearing Loss

ABSTRACT The active ingredient of the traditional Chinese medicine comfrey is shikonin, a naphthoquinone compound. The focus of this study was to investigate the effect of shikonin on the proliferation, invasion, migration, and chemoresistance of non-small cell lung cancer (NSCLC) cells, and to explore its underlying molecular biological mechanisms. The results show that shikonin inhibited the viability, proliferation, invasion, and migration of NSCLC cells A549 and PC9, and induced apoptosis. As the inhibitor of pyruvate kinase M2 (PKM2), a key enzyme in glycolysis, shikonin inhibited glucose uptake and the production of lactate, the final metabolite of aerobic glycolysis. In vivo chemotherapeutic assay showed that shikonin reduced the tumor volume and weight in NSCLC mice model and increased the sensitivity to cisplatin chemotherapy. Histoimmunology experiments showed the combination of shikonin and cisplatin downregulated the expression of PKM2 and its transcriptionally regulated downstream gene glucose transporter 1 (Glut1) in tumor tissue. In an assessment of glucose metabolism, micro-PET/CT data showed a combination of shikonin and cisplatin inhibited the fluorodeoxy glucose (18F-FDG) uptake into tumor. Since exosomal PKM2 affected the sensitivity to cisplatin in NSCLC cells, we also demonstrated shikonin could inhibit exosome secretion and exosomal PKM2 through the administration of exosomal inhibitor GW4869. Furthermore, shikonin sensitized cisplatin treatment by reducing the extracellular secretion of exosomal PKM2. In conclusion, we suggest that shikonin not only inhibits PKM2 intracellularly but also reduces glycolytic flux and increases cisplatin sensitivity through the exosomal pathway. GRAPHICAL ABSTRACT

https://www.tandfonline.com/doi/pdf/10.1080/21655979.2022.2086378?needAccess=true

Shikonin inhibited glycolysis and sensitized cisplatin treatment in non-small cell lung cancer cells via the exosomal pyruvate kinase M2 pathway

Conclusion. The results of this study indicate that diabetes causes up-regulation of vascular endothelial growth factor (VEGF), inducible nitric oxide synthase (iNOS), and endothelial nitric oxide ...

Expression of VEGF, iNOS, and eNOS is increased in cochlea of diabetic rat.

The present study aimed to investigate the impact of overexpression of long noncoding RNA PEG10 (lncRNA PEG10) on the proliferation, invasion and metastasis of hypopharyngeal squamous cell carcinoma (HSCC). Quantitative reverse transcription polymerase chain reaction was used to quantify lncRNA PEG10 expression levels in HSCC tumor tissues samples, para-carcinoma tissue samples and the HSCC FaDu cell line. Cell proliferation assays, Transwell invasion assays and wound healing assays were used to evaluate the effects of lncRNA PEG10 on FaDu cells in vitro. In 56 eligible patients, lncRNA PEG10 was expressed at higher levels in HSCC tumor tissues compared with para-carcinoma tissues, and significant associations were observed between increased tumor expression of lncRNA PEG10 and primary tumor size, lymph node status and tumor node metastasis stage. In the in vitro experimental studies, enhanced expression of lncRNA PEG10 was significantly associated with increased proliferation, invasion and metastasis of FaDu cells. lncRNA PEG10 was upregulated in HSCC, and its overexpression in HSCC cells promoted an increase in the tumorigenic activities of proliferation, invasion and migration. The potential underlying mechanisms require investigation in future studies.

/pdf/overexpression-of-long-noncoding-rna-peg10-promotes-199dwsn79r.pdf

Overexpression of long noncoding RNA PEG10 promotes proliferation, invasion and metastasis of hypopharyngeal squamous cell carcinoma.

Background: Geranylgeranylacetone (GGA) has the ability to induce heat shock proteins and to protect cells from apoptotic insults. This study aims to investigate whether GGA has a p

Protective effect of geranylgeranylacetone on cisplatin ototoxicity.

NGR-modified PEG-PLGA micelles containing Shikonin enhance targeting of dendritic cells for therapy of allergic rhinitis.

Conclusions: Vestibular function disorders were widespread among nasopharyngeal carcinoma (NPC) patients. The radiation doses to the inner ears were associated with the incidence of vestibular function disorders, but the correlations were mild. The inflammatory responses and possible resolution obstacles of inflammation participated in persistent vestibular function disorders after irradiation. Objectives: To investigate the incidence of vestibular function disorders in NPC patients after irradiation and potential mechanisms. Methods: Patients who received radical intensity-modulated radiotherapy for their NPC were recruited. The serum levels of IL-6 and IL-17 were detected by ELISA method. Vestibular evoked myogenic potential (VEMP) tests were used to evaluate vestibular function and correlation analyses were used to analyze the potential mechanisms of vestibular function disorders. Results: Thirty-eight patients were included. The incidences of abnormal ocular VEMP (oVEMP) and cervical VEMP (cVE...

Vestibular function disorders and potential mechanisms in irradiation nasopharyngeal carcinoma patients.

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