Influencing factors and hemodynamic study of initial and sustained orthostatic hypotension in middle-aged and elderly patients.

Orthostatic hypotension (OH) is a common autonomic disorder. This study aimed to investigate the influencing factors and hemodynamic mechanisms of initial and sustained OH in middle-aged and elderly patients. The authors analyzed the clinical characteristics and hemodynamic variables of patients aged ≥ 50 years according to the various forms of OH, diagnosed by an active orthostatic test using the CNAP monitor. The study included 473 participants; 119 (25.2%) patients had initial (54, 45.4%) or sustained (65, 54.6%) OH. Age, comorbidities, or medications did not differ significantly between the initial OH and non-OH groups. Sustained OH was associated with age and diabetes (p = .003 and p = .015, respectively). Hemodynamic analysis revealed higher cardiac output (CO) in the sustained OH group within 15 s than in the non-OH and initial OH groups (both p < .001); no difference in CO was observed between the initial OH and non-OH groups. The systemic vascular resistance (SVR) in both initial OH and sustained OH groups within 15 s was lower than that in the non-OH group (both p < .001). No differences in SVR at 3 min were observed between the initial OH and non-OH groups. The SVR at 3 min in the sustained OH group was significantly lower than in non-OH and initial OH groups (both p < .001). Age and diabetes emerged as the independent risk factors associated with sustained OH. Initial OH is associated with a mismatch of increase in CO and decrease in SVR. Sustained OH is mainly associated with sustained inadequate adjustment in SVR.

ADAR1 Alleviates Inflammation in a Murine Sepsis Model via the ADAR1-miR-30a-SOCS3 Axis.

Adenosine deaminase acting on double-stranded RNA 1 (ADAR1) mediates adenosine-to-inosine (A-to-I) RNA editing events. ADAR1 is highly expressed in "septic" macrophages and in small intestinal tissues of mice with sepsis. Overexpression of ADAR1 suppresses inflammation and intestinal damage. However, the specific underlying mechanism is unclear. This study was conducted to explore how microRNA (miRNA) regulates the anti-inflammatory mechanism of macrophages following ADAR1 upregulation. A murine sepsis model was established by cecal ligation and puncture (CLP). Mice were randomly assigned to sham, CLP, and CLP+ADAR1 groups. Hematoxylin and eosin (HE) staining and fluorescence isothiocyanate-dextran were used to evaluate intestinal injury and permeability. Quantitative reverse transcription-polymerase chain reaction (qRT-PCR), western blotting, and Luminex assays were performed to detect changes in the expression of inflammatory cytokines. Adenoviruses were used to express ADAR1 in RAW 264.7 cells. Ribonucleoprotein immunoprecipitation analysis was conducted to detect the binding of ADAR1 and miRNAs. A dual-luciferase reporter assay was used to detect the binding of miRNAs and regulatory factors. We observed that ADAR1 significantly increased the expression of suppressor of cytokine signaling 3 (SOCS3) in macrophages and reduced the expression of interleukin-6 in macrophages and the serum, thereby reducing intestinal permeability and mucosal injury in mice with sepsis. The RNA-ribonucleoprotein immunoprecipitation binding assay and qRT-PCR demonstrated a direct interaction between ADAR1 and pri-miR-30a. The luciferase assay demonstrated that SOCS3 was significantly inhibited by miR-30a-5p, the mature product of miR-30a. Thus, ADAR1 exerts a protective effect against sepsis by reducing inflammation and organ damage via the ADAR1-miR-30a-SOCS3 axis.

The Pneumatization and Adjacent Structure of the Posterior Superior Maxillary Sinus and Its Effect on Nasal Cavity Morphology.

BACKGROUND The aim of this study was to observe the pneumatization degree and adjacent structure of the posterior superior maxillary sinus (PSMS) and its effect on nasal cavity morphology. MATERIAL AND METHODS The study included a total of 103 cases whose paranasal sinus CT scans had been analyzed. The pneumatization of the PSMS and its relationship with posterior ethmoid sinus (PEs) and sphenoid sinus (SS) were observed. The effects of the pneumatization of PSMS on nasal cavity width and morphology also were evaluated. RESULTS 1) The PSMS was adjacent to orbit or middle nasal meatus (MNM) as type I in 5.82% of cases. The PSMS was adjacent to the orbit and superior nasal meatus (SNM) as follows: the superior part of medial wall of maxillary sinus (MMS) was not abutting on PEs as type II (4.35%) and abutting on PEs as type III (85.9%). If the type III was not accompanied by MMS shift toward medial it was identified as type IIIa (33.50%), and if it was accompanied MMS shift toward medial, it was identified as type IIIb (45.63%). The ethmomaxillary sinus (EMS) was identified as type IIIc (6.80%). The PSMS directly abutted on the SS as type IV in (3.88%). 2) The higher the degree of the pneumatization of PSMS was, the narrower the width of the upper part of the posterior nasal cavity (p<0.05 respectively). CONCLUSIONS The relationship of PSMS with the orbit, SNM, PEs, and SS should be identified pre-operation; it is important for safety and complete removal of retromaxillary lesions during endoscopic sinus surgery. The pneumatization degree of PSMS also should be considered as it can influence the morphology of posterior nasal cavity.

[Differential proteomics on synthetic antimicrobial decapeptide against Streptococcus mutans].

OBJECTIVE: To compare the protein profiles between decapeptide-treated and untreated planktonic cells of Streptococcus mutans (S. mutans) by differential proteomic analysis to determine and identify the key proteins. METHODS: In our previous study, we investigated decapeptide (KKVVFKVKFK-NH2), which was a novel adenosine monophosphate. Compared with other oral pathogens tested, decapeptide had a preferential antibacterial activity against S. mutans. It also inhibited S. mutans biofilm formation and reduced the one-day developed biofilm. In the present study, we first synthesized decapeptide, and then compared the protein profiles between decapeptide-treated and untreated planktonic cells of S. mutans by two-dimensional gel electrophoresis and matrix-assisted laser desorption ionization time-of-flight mass spectrometry. We also verified different expressions of key protein enolase in the protein level. RESULTS: The results showed that decapeptide altered the protein expression of planktonic S. mutans. These proteins were functionally involved in carbohydrate degradation by glycolysis, protein folding, conjunction, transport, translation, adenosine triphosphate binding, protein binding, sequence-specific DNA binding, transcription factor activity, and two-component response regulator activity. Western blot results showed that enolase protein expression decreased obviously in decapeptide-treated cells of S. mutans. CONCLUSION: The protein expression of S. mutans significantly changed after synthetic antimicrobial decapeptide treatment, suggesting that decapeptide may present a preferential effect on oral caries by changing the expression of certain key proteins, such as enolase protein.

WITHDRAWN: Effect of blood glucose fluctuation on the function of rat pancreatic islets in vivo.

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Disruption of connective tissue growth factor by short hairpin RNA inhibits collagen synthesis and extracellular matrix secretion in hepatic stellate cells.

PURPOSE: Connective tissue growth factor (CTGF) plays a key role in the pathogenesis of liver fibrosis. This study aimed at investigating that the disruption of CTGF expression by short hairpin RNA (shRNA) could modulate the production of fibrosis-related components in hepatic stellate HSC-T6 cells. METHODS: Three plasmids expressing individual shRNA were constructed and transfected into HSC-T6 cells respectively. The levels of CTGF and transforming growth factor beta1 (TGF-beta1) expression were determined by reverse transcriptase-polymerase chain reaction and Western blot assays. Furthermore, the production of collagens and extracellular matrix (ECM) proteins, including type III procollagen (PC III), type IV collagen (collagen IV), laminin (LN) and hyaluronic acid (HA) in the CTGF-disrupted cells, were analysed by radioimmunoassay. RESULTS: Following transfection with the pEGFP-CTGFshRNA1, the expression of CTGF was disrupted in HSC-T6 cells. While the knockdown of CTGF expression failed to modulate the expression of TGF-beta1, it did significantly reduce the production of PC III, collagen IV, LN and HA by HSC-T6 cells. CONCLUSION: Our data suggest that shRNA-mediated disruption of CTGF expression can attenuate ECM synthesis. Potentially, our findings may aid in the design of a CTGF-based new therapy for treatment of hepatic fibrosis.