A comparative study of ultrasound cycloplasty and endoscopic cyclophotocoagulation in the treatment of secondary glaucoma.

To compare the clinical efficacy of ultrasound cycloplasty (UCP) and endoscopic cyclophotocoagulation (ECP) in the treatment of secondary glaucoma. In a 12-month prospective single-center study, 22 patients with secondary glaucoma were treated by high-intensity focused ultrasound (HIFU), and 23 patients with secondary glaucoma were treated by a semiconductor laser. At the final follow-up, the two groups' surgical outcomes were compared. A complete success was defined as an intraocular pressure (IOP) reduction of at least 20% from baseline and an IOP of > 5 mmHg and ≦ 21 mmHg, while a qualified success was defined as an IOP reduction of at least 20% from baseline and an IOP of > 5 mmHg. The secondary outcome was the average IOP, number of drugs, and complications at each follow-up compared with the baseline. The average preoperative IOPs in the UCP and ECP groups were 36.4 ± 9.5 mmHg (n = 2.3 drops, n = 0.2 tablets) and 34.5 ± 11.7 mmHg (n = 2.0 drops, n = 0.3 tablets), respectively. In the last follow-up, the success rate of UCP was 54% (with a decrease of 32%) and that of ECP was 65% (with a decrease of 35%), and the P-value between the two groups was > 0.05. However, there was a difference in the average IOP between these two groups 1 day and 1 week after the operation, and the IOP reduction efficiency in the ECP group was better. However, the amount of drug used after these two surgeries was significantly reduced. There were fewer postoperative complications in the UCP group (18 cases) than in the ECP group (35 cases). Both UCP and ECP can effectively reduce IOP in secondary glaucoma, and ECP has a better effect at the early stages. However, UCP has higher safety and tolerance for patients.

The Neuropeptide-Related HERC5/TAC1 Interactions May Be Associated with the Dysregulation of lncRNA GAS5 Expression in Gestational Diabetes Mellitus Exosomes.

OBJECTIVE: The goal of this work was to look at the expression and probable role of exosomal long noncoding RNA (lncRNA) GAS5 in gestational diabetes mellitus (GDM), as well as forecast the importance of its interaction with neuropeptides in the progression of the disease. METHODS: We divided 44 pregnant women visiting the obstetric outpatient clinics at the Affiliated Hospital of Guilin Medical College from January 2021 to December 2021 into healthy and GDM groups. We measured the expression levels of the lncRNA GAS5 in peripheral blood using PCR and compared the expression levels between the 2 groups. The Gene Expression Omnibus (GEO) database and the R software were used to analyse the differences in the genes expressed in the amniotic fluid cells in the GDM and normal groups. catRAPID was used to identify potential target proteins for GAS5. Key neuropeptide-related proteins and potential target proteins of GAS5 were extracted, and protein interaction networks were mapped. AlphaFold 2 was used to predict the structure of the target protein. The ClusPro tool was used to predict protein-protein interactions. ZDOCK was used to further confirm the protein-nucleic acid docking. RESULTS: The lncRNA GAS5 was downregulated in the peripheral blood of pregnant women with GDM compared with normal pregnant women. The subcellular localization sites of GAS5 were the nucleus, cytoplasm, and ribosome; in addition, GAS5 was present in exosomes. Intercellular interactions, including neuropeptide receptors, were increased in the amniotic fluid cells of patients with GDM. Venn diagram analysis yielded seven neuropeptide-related proteins and three GAS5 target proteins. Among them, HERC5/TAC1 interacted and GAS5 docked well with HERC5. CONCLUSION: The lncRNA GAS5 in the peripheral blood exosomes in patients with GDM may be a new target for the detection of GDM, and the interaction between GAS5 and HERC5/TAC1 may be involved in the pathogenesis of GDM.

Development of methods for detecting the fate of mesenchymal stem cells regulated by bone bioactive materials.

The fate of mesenchymal stem cells (MSCs) is regulated by biological, physical and chemical signals. Developments in biotechnology and materials science promoted the occurrence of bioactive materials which can provide physical and chemical signals for MSCs to regulate their fate. In order to design and synthesize materials that can precisely regulate the fate of MSCs, the relationship between the properties of materials and the fate of mesenchymal stem cells need to be clarified, in which the detection of the fate of mesenchymal stem cells plays an important role. In the past 30 years, a series of detection technologies have been developed to detect the fate of MSCs regulated by bioactive materials, among which high-throughput technology has shown great advantages due to its ability to detect large amounts of data at one time. In this review, the latest research progresses of detecting the fate of MSCs regulated by bone bioactive materials (BBMs) are systematically reviewed from traditional technology to high-throughput technology which is emphasized especially. Moreover, current problems and the future development direction of detection technologies of the MSCs fate regulated by BBMs are prospected. The aim of this review is to provide a detection technical framework for researchers to establish the relationship between the properties of BMMs and the fate of MSCs, so as to help researchers to design and synthesize BBMs better which can precisely regulate the fate of MSCs.

[Energy Demand and Its Regulatory Mechanism during Folliculogenesis].

The growth and development of follicles are regulated by genes,hormones and growth factors autocrined and paracrined from granulosa cells,theca cells,and oocytes.Products of glycolysis from granulosa cells such as pyruvate and lactate are one of the main energy sources,which play an important role during folliculogenesis and follicle maturity.Studies on the changes of the products and rate-limiting enzymes during granulosa cells' glycolysis help to clarify the molecular mechanism of energy demand in folliculogenesis and guide the clinical treatment of infertility due to abnormal follicular development.This article reviews recent research advances in the energy demand and regulatory mechanism in different states of folliculogenesis.

"Pill-in-the-Pocket" Treatment of Propafenone Unmasks ECG Brugada Pattern in an Atrial Fibrillation Patient With a Common SCN5A R1193Q Polymorphism.

Background: "Pill-in-the-pocket" (PIP) treatment with type IC drugs for cardioversion of recent-onset atrial fibrillation (AF) has been recommended in guidelines. Major adverse effects have been often reported, and the underlying mechanisms are proposed to be associated with the genetic backgrounds. Methods and Results: A male patient was treated with PIP approach (propafenone 600 mg.po) for the conversion of new onset AF. His symptoms got worse and referred to emergency room; ECG showed a typical Brugada syndrome (BrS) type I ECG pattern with sinus rhythm. Genetic screening identified a common SCN5A polymorphism R1193Q. Propafenone blockade of INa was studied in HEK293 cells expressed SCN5A R1193Q channel and WT channel using patch clamp techniques. There was no significant difference in peak current and steady-state gating parameters between R1193Q and WT at baseline. At clinically relevant concentration of 2 µmol/L propafenone, use-dependent block (UDB) of INa was more pronounced in R1193Q versus WT (44.2 ± 7.2 versus 24.8 ± 5.7% at the frequency of 2 Hz, P < 0.05); IC50 of UDB was 2.9 ± 0.7 µmol/L for R1193Q and 8.1 ± 1.8 µmol/L for WT, respectively. Propafenone produced more left shift of steady-state inactivation and slower recovery from inactivation in R1193Q compared with WT. Conclusion: A common SCN5A polymorphism R1193Q enhances UDB by propafenone and predisposes the patients to drug-induced BrS with PIP treatment. Our data suggest that R1193Q polymorphism is likely to be a genetic marker for the major adverse effects associated with propafenone PIP approach for AF patients' management. Ajmaline challenge to rule out the presence of BrS should be considered prior to propafenone PIP therapy in AF patients who are identified to have R1193Q polymorphism.

Two lytic transglycosylases of Xanthomonas campestris pv. campestris associated with cell separation and type III secretion system, respectively.

The lytic transglycosylases (LTs) are important enzymes that degrade peptidoglycan of the bacterial cell wall and affect many biological functions. We present here that XC_0706 and XC_3001 are annotated as the LTs in Xanthomonas campestris pv. campestris. XC_0706 is associated with virulence and plays a pivotal role in cell division. Mutation on XC_3001 reduced hypersensitive response induction and the translocation of type III effector, but did not affect the function of the type II secretion system. Further studies showed that multiple LTs genes contribute to efficiency of the type III secretory system in X. campestris pv. campestris.

Influences of 3-methylcholanthrene, phenobarbital and dexamethasone on xenobiotic metabolizing-related cytochrome P450 enzymes and steroidogenesis in human fetal adrenal cortical cells.

AIM: To explore the influence and possible mechanism of xenobiotics on adrenal steroidogenesis during fetal development. METHODS: Primary human fetal adrenal cortical cells were prepared, cultured and treated with 3-methylcholanthrene, phenobarbital and dexamethasone. The activities of 7-ethoxyresorufin O-dealkylase, benzphetamine, aminopyrine and erythromycin N-demethylases were measured by enzyme assays. At the same time, quantitative analysis of steroid hormones cortisol, aldosterone, testosterone and progesterone were carried out in cultural medium by radioimmunoassays. RESULTS: The activities of benzphetamine and aminopyrine N-demethylase were increased in the cultural fetal adrenal cells treated with phenobarbital (0.25-1 mmol/L) for 24 h. Dexamethasone (25-100 micromol/L) also increased the activity of erythromycin N-demethylase. The activity of 7-ethoxyresorufin O-dealkylase was undetected in the cells treated without and with 3-methylcholanthrene (0.5-2 micromol/L). Meanwhile, the contents of medium cortisol, aldosterone and progesterone were decreased after treatment with 3-methylcholanthrene. Cortisol, aldosterone and progesterone concentrations were also slightly decreased with phenobarbital. Dexamethasone enhanced the productions of cortisol and progesterone remarkably. The trend of testosterone concentration was uncertain after 3-methylcholanthrene, phenobarbital or dexamethasone treatment. CONCLUSION: 3-Methylcholanthrene, phenobarbital or dexamethasone could interfere with the synthesis of cortisol, aldosterone and progesterone in primary human fetal adrenal cortical cells, which likely act through xenobiotic metabolizing-related cytochrome P450 isoform activation.