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Apolipoprotein E (ApoE) gene knockout (KO) mice develop hearing loss, as well as hair cell damage in the inner ear. Furthermore, the hearing loss and hair cell damage may be caused and exacerbated by hyperlipidemia and atherosclerosis. We are therefore seeking an effective treatment to protect the inner ear in ApoE-KO mice. ApoE-KO mice fed with an atherosclerotic diet were treated with simvastatin or with Strauss Heartdrops. The auditory brainstem responses were recorded, and plasma lipid levels and inner ear histology were examined. ApoE-KO and wild-type C57BL/6J mice fed with a normal chow diet served as controls. Compared to ApoE-KO mice fed only the atherosclerotic diet, ApoE-KO mice treated with simvastatin had no significant hearing loss and less severe atherosclerosis and hair cell damage in the inner ear. However, ApoE-KO mice treated with Strauss Heartdrops developed significant hearing loss and severe atherosclerosis and hair cell damage in the inner ear. These results demonstrate that statins may prevent hearing loss and inner ear damage in ApoE-KO mice by reducing the atherosclerotic lesions and levels of glucose, cholesterol, low-density lipoprotein, and triglyceride. Statins could be used to treat hearing loss associated with hyperlipidemia.

A low pepsinogen (PG) I/II ratio can be used to detect atrophic gastritis (AG). Recent research has found that the PG I/II ratio is associated with several nutritional and metabolic disorders. The aim of this study is to investigate the relationship between the PG I/II ratio and biochemical markers in a Chinese population.In total, 1896 participants in a gastric cancer screening program underwent a health screening test that included assessment of serum pepsinogens. Subjects with PG I/II < 3.0 were considered as having atrophic gastritis. Associations between the PG I/II ratio and biochemical markers reflecting glucose and lipid metabolism, liver, kidney and thyroid functions were evaluated using SPSS software version 20.The prevalence of atrophic gastritis was 5.3% and increased with age but did not differ between sexes. Albumin, ferritin, and total and direct bilirubin were significantly lower in patients with AG than in those without AG, whereas age, total bile acid, and amylase were significantly higher. Albumin, ferritin, and triglyceride correlated positively with the PG I/II ratio, while age, total bile acid, blood urea nitrogen, amylase, aspartate aminotransferase, creatine kinase, and lactate dehydrogenase correlated inversely with the PG I/II ratio. Logistic regression analysis demonstrated that age, total bile acid, total protein, and ferritin correlated independently with AG.Low PG I/II ratio is not only a marker of atrophic gastritis but also an indicator of nutritional and metabolic status. Special attention should be paid to the metabolism of iron, protein, and bile acid in patients with a low PG I/II ratio.

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ObjectiveTo investigate the serum level of cystatin C (CysC), ischemia-modified albumin (IMA), and lipoprotein-associated phospholipase A2 (LP-PLA2) in patients with type 2 diabetes mellitus (T2DM) and with lower extremity atherosclerotic occlusive disease (LEASOD) and their correlation.MethodsFrom March 2017 to December 2019, 110 patients with T2DM with LEASOD, who were treated in our hospital, were selected as the observation group. One hundred ten healthy persons who received medical examination in our hospital during the same period were selected as the control group. Serum CysC, IMA, LP-PLA2, and ankle-brachial index (ABI) were detected in each group. According to the ABI index, the observation group was divided into three subgroups, namely, the mild group (n = 45), the moderate group (n = 42), and the severe group (n = 23). Pearson correlation analysis was used to analyze the relationship between serum CysC, IMA, and LP-PLA2 levels in patients with T2DM with LEASOD and their condition. The receiver operator characteristic (ROC) curve was used to analyze the diagnostic value of serum CysC, IMA, and LP-PLA2 levels in patients with T2DM with LEASOD.ResultsThe serum levels of CysC, IMA, and LP-PLA2 in the observation group were higher than those in the control group (p &lt; 0.05). The serum levels of CysC, IMA, and LP-PLA2 in the severe and the moderate group were higher than those in the mild group, and the serum levels of CysC, IMA, and LP-PLA2 in the severe group were higher than those in the moderate group (p &lt; 0.05). Pearson correlation analysis showed that CysC, IMA, and LP-PLA2 levels were all negatively correlated with ABI (r = −0.802, r = −0.757, r = −0.764, p &lt; 0.001). The ROC curve results showed that the area under the curve (AUC) of serum CysC in the diagnosis of T2DM with LEASOD was 0.806, and the best cut-off value was 1.74 mg/L. The AUC of serum IMA for diagnosis of T2DM with LEASOD was 0.772, and the best cut-off value was 92.58 g/L. The AUC of serum LP-PLA2 in the diagnosis of T2DM with LEASOD was 0.781, and the best cut-off value was 544.86 ng/L. The AUC of the three combined diagnoses of T2DM with LEASOD was 0.863.ConclusionSerum levels of CysC, IMA, and LP-PLA2 were increased in patients with T2DM with LEASOD. Serum CysC, IMA, and LP-PLA2 are closely related to the severity of the disease. The higher the serum levels of CysC, IMA, and LP-PLA2, the more serious the degree of lower extremity arteriosclerosis occlusion, which can be used as an important serum marker to monitor the severity of T2DM with LEASOD. The combined detection of serum CysC, IMA, and LP-PLA2 has good diagnostic value for patients with T2DM with LEASOD.

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<b><i>Background:</i></b> Many studies have confirmed that circular RNA (circRNA) is an important target for regulating human disease progression. This study aimed to explore the role of circ_0068087 in diabetic nephropathy (DN) progression. <b><i>Methods:</i></b> High glucose (HG)-induced renal tubular cells (HK2) were used to mimic DN cell models in vitro. The expression levels of circ_0068087, microRNA (miR)-106a-5p, and Rho-associated coiled-coil-containing kinase 2 (ROCK2) were detected by quantitative real-time PCR. Cell proliferation and apoptosis were examined by cell counting kit-8 assay, 5-ethynyl-2′-deoxyuridine assay, colony formation assay, and flow cytometry. The protein levels were examined by Western blot analysis. Cell oxidative stress was assessed by measuring MDA level and SOD activity, and cell inflammation was evaluated by detecting the concentrations of inflammatory factors. RNA interaction was verified by dual-luciferase reporter assay and RNA pull-down assay. <b><i>Results:</i></b> The present study showed that circ_0068087 was highly expressed in the serum of DN patients and HG-induced HK2 cells. Interference of circ_0068087 alleviated HG-induced apoptosis, oxidative stress, inflammation, and fibrosis in HK2 cells, while accelerated cell proliferation. miR-106a-5p could be sponged by circ_0068087, and its inhibitor eliminated the regulation of circ_0068087 knockdown on HG-induced HK2 cell injury. ROCK2 was a target of miR-106a-5p, and its expression was suppressed by circ_0068087 knockdown. miR-106a-5p overexpression suppressed HG-induced HK2 cell injury, and this effect was reversed by ROCK2 upregulation. <b><i>Conclusion:</i></b> Our data indicated that circ_0068087 downregulation mitigated HG-induced HK2 cell injury through the miR-106a-5p/ROCK2 axis, providing a potential circRNA-targeted therapy for DN.

BackgroundVisceral leishmaniasis (VL), caused by the protozoan Leishmania species, is the most severe form of leishmaniasis. The parasite migrates to the internal organs such as the liver, spleen, and bone marrow, and if left untreated, will almost always cause the host to die [1]. Due to polyclonal B cells activation, VL may present signs and symptoms resembling those of rheumatic diseases, especially systemic lupus erythematosus (SLE) [2-4]. This can sometimes lead to mis-diagnosis and treatment of corticosteroids.ObjectivesTo analyze 27 Chinese VL patients retrospectively and focused on their autoimmune findings that could help clinicians to differentiate VL from SLE.Methods27 in-hospitalized VL patients in our hospital from 2006 to 2015 were analyzed. VL was diagnosed by the presence of high titers of anti-leishmania antibodies in the blood or by demonstration of intracellular parasites on bone marrow aspiration. All patients were negative for hepatitis B, hepatitis C and human immunodeficiency viruses. Autoimmune antibodies were detected. Levels of serum globulins, complement C3, C4 and RF were evaluated. Coagulation parameters, including prothrombin time (PT) and activated partial thromboplastin time (APTT) were also tested.ResultsThe basic characteristics and laboratory findings of the 27 patients were summarized in Table 1. All patients had hepatosplenomegaly. 38.9% had positive ANA, but the titer was no more than 1:320. None of the patients had positive anti-Sm antibody and only 1 had anti-dsDNA antibody. 89.5% had increased IgG level and none had decreased C3 or C4.All patients were cured with sodium stibogluconate, and ANA titers decreased after treatment.ConclusionVL may mimic symptoms of SLE due to polyclonal activation of B cells. However, hepatosplenomegaly is a common symptom seen in VL but not so common in SLE. Furthermore, VL patients don’t have typical autoantibodies of SLE, their ANA titer are normal to low and they tend to have normal complements, which could help clinicians to differentiate these two diseases.Table 1Basic characteristics and clinical manifestations of VL patientsSex (Femal/Male)4/23Age (median, range)37 (9-59)Disease duration (months) (median, range)1 (0.17-24)Anti- leishmania antibodies positive27Parasites positive in bone marrow24Fever25Hepatosplenomegaly27Weight loss14Anemia26Leucocytopenia23Thrombocytopenia20Prolonged APTT12/21Prolonged PT12/21Positive ANA7/18References[1] Martins-Melo FR, Lima Mda S, Ramos ANAN Jr., and, et al. Mortality and case fatality due to visceral leishmaniasis in Brazil: a nationwide analysis of epidemiology, trends and s patial patterns. PLoSOne. 2014; 9: e93770.[2] Ozlem Guzel Tunccan, Abdurrahman Tufan, Gülçin Telli, et al. Visceral Leishmaniasis Mimicking Autoimmune Hepatitis, Primary Biliary Cirrhosis, and Systemic Lupus Erythematosus Overlap. Korean J Parasitol. 2012; 50(2): 133–6[3] Voulgarelis M, Voulgari PV, Serelis J, et al. Visceral leishmaniasis mimicking systemic lupus erythematosus. J Clin Rheumatol. 2010;16(4): 203-4.[4] Drosos AA,...