Ultrasound-guided intersphincteric space block combined with spinal anesthesia for hemorrhoidectomy: a randomized clinical trial.

BACKGROUND: We aimed to compare the analgesic effects and incidence of urinary retention between ultrasound-guided intersphincteric space block combined with low-dose ropivacaine spinal anesthesia and conventional-dose ropivacaine spinal anesthesia post-hemorrhoidectomy. METHODS: Fifty patients aged 20-65 years who underwent elective hemorrhoidectomy were stochastically assigned to one of two groups. Spinal anesthesia was induced with 8 mg ropivacaine, combined with ultrasound-guided intersphincteric space block in the treatment group. Spinal anesthesia was induced with 12 mg ropivacaine in the control group. The primary outcome was the postoperative pain score, measured using the Visual Analog Scale (VAS) at 4, 8, 12, 24, and 48 hours and at the first defecation postoperatively. Secondary outcomes included urinary retention, extent of anal sphincter relaxation, and the time required to lift the lower limbs out of bed postoperatively. RESULTS: The treatment group showed markedly lower VAS scores than those of the control group at 8, 12, 24, and 48 h, and at the first postoperative defecation time (P<0.05). The incidence of urinary retention was considerably lower in the treatment group than in the control group (24% vs. 52%, P=0.04). No remarkable difference in the degree of anal sphincter relaxation was observed between the two groups (P=0.556). The time taken by the treatment group patients to lift their lower limbs off the bed was much shorter than that in the control group (1.3±0.6 h vs. 3.2±1.2 h, P<0.001). CONCLUSIONS: Ultrasound-guided intersphincteric space block combined with low-dose ropivacaine spinal anesthesia provides good anesthesia and analgesia for hemorrhoidectomy.

Anisotropic Elastomer Ionomer Composite-Based Strain Sensors: Achieving High Sensitivity and Wide Detection for Human Motion Detection and Wireless Transmission.

Anisotropic strain sensors capable of multidirectional sensing are crucial for advanced sensor applications in human motion detection. However, current anisotropic sensors encounter challenges in achieving a balance among high sensitivity, substantial stretchability, and a wide linear detection range. To address these challenges, a facile freeze-casting strategy was employed to construct oriented filler networks composed of carbon nanotubes and conductive carbon black within a brominated butyl rubber ionomer (iBIIR) matrix. The resulting anisotropic sensor based on the iBIIR composites exhibited distinct gauge factors (GF) in the parallel and vertical directions (GF∥ = 4.91, while GF⊥ = 2.24) and a broad linear detection range over a strain range of 190%. This feature enables the sensor to detect various human activities, including uniaxial pulse, finder bending, elbow bending, and cervical spine movements. Moreover, the ion-cross-linking network within the iBIIR, coupled with strong π-cation interactions between the fillers and iBIIR macromolecules, imparted high strength (12.3 MPa, nearly twice that of pure iBIIR) and an ultrahigh elongation at break (>1800%) to the composites. Furthermore, the sensor exhibited exceptional antibacterial effectiveness, surpassing 99% against both Escherichia coli and Staphylococcus aureus. Notably, the sensor was capable of wireless sensing. It is anticipated that anisotropic sensors will have extensive application prospects in flexible wearable devices.

RNA-seq analysis revealed genes associated with neuropathic pain induced by chronic compressive injury in interferon regulatory factors 4 knockout mice.

OBJECTIVE: To explore the differential expression of genes between wild-type chronic compressive injury (CCI) mice (WT-CCI) and interferon regulatory factors 4 (IRF4) knockout CCI mice (KO-CCI) by RNA-seq analysis of the mouse spinal cord. METHODS: RNA-seq analysis of the spinal cord tissue of the chronic sciatic nerve ligation mice and Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analyses were used. RESULTS: A total of 104 genes were up-regulated and 116 genes were down-regulated in spinal cord of the mice in IRF4 knockout (KO-CCI) group compared with that in the wild-type CCI (WT-CCI) group. There were 1472 differentially expressed genes in the biological process group, 62 differentially expressed genes in the cellular component group, and 163 differentially expressed genes in the molecular function group in KO-CCI mice. A total of 14 genes related to inflammatory reactions were differentially expressed. Real-time PCR results confirmed that Pparg and Grpr mRNA expression was up-regulated and Arg 1 and Ccl11 mRNA expression was down-regulated in the KO-CCI group. CONCLUSION: IRF4 is involved in neuropathic pain in CCI mice, IRF4 may participate in neuropathic pain by regulating Grpr, Mas1, Galr3, Nos2, Arg1, Ccl11, Ptgs2, S100a8, Pparg, Cd40, Has2, Gpr151, Il123a, Capns2, Ankrd1, Ccnb1, and Nppb genes.

Retrospective analysis on the efficacy of epidural labor analgesia on early breast feeding after vaginal delivery.

BACKGROUND: Breastfeeding is essential for infants and mothers. Epidural labor analgesia is used frequently to alleviate pain during vaginal delivery. Studies have found that epidural labor analgesia potentially have negative effects on postpartum breastfeeding. However, the efficacy of epidural labor analgesia on early breastfeeding after vaginal delivery is unclear. Therefore, a retrospective analysis was performed to illuminate the efficacy of epidural labor analgesia on postpartum breast feeding. METHODS: A total of 392 women who received vaginal delivery in the Second People's Hospital of Foshan from July 2022 to June 2023 were selected for this study, and all women received epidural labor analgesia and were divided into three groups according to the efficacy of labor analgesia. There were three groups: parturients with VAS scores < 3 were divided into Group E (n = 192), parturients with VAS scores 4-6 were divided into Group M (n = 127), and parturients with VAS scores > 7 were divided into Group P (n = 73). The labor process, lactation initiation time, and incidence of delayed onset of lactation were analyzed. The lactation volume and time and LATCH score at 24, 48 and 72 h after vaginal delivery were also analyzed. RESULTS: There was no significant difference in labor process times among the three groups (P > 0.05). The cases of prolactin use in Group M were less than those in Group E and Group P, with a significant difference (all P < 0.05). There was no significant difference in cases of prolactin use between Group E and Group P (P > 0.05). The lactation initiation time in Group M was significantly shorter than those in Group E and Group P (all P>0.05). There was no significant difference in lactation initiation time after vaginal delivery between Group E and Group P (P>0.05). The incidence of delayed onset of lactation in Group M was significantly lower those that in Group E and Group P (all P < 0.05). There was no statistically significant difference in the incidence of delayed onset of lactation between Group E and Group P (P > 0.05). The lactation volumes at 24, 48 and 72 h after vaginal delivery in Group M were significantly higher than those in Group E and Group P (all P < 0.05). There was no significant difference in lactation volume at 24, 48 and 72 h after vaginal delivery between Group E and Group P (P > 0.05). The lactation times at 24, 48 and 72 h after vaginal delivery in Group M were significantly higher than those in Group E and Group P (all P < 0.05). There was no significant difference in lactation times at 24, 48 and 72 h after vaginal delivery between Group E and Group P (P > 0.05). There was no significant difference in LATCH scores at 24, 48 and 72 h after vaginal delivery among the three groups (all P > 0.05). CONCLUSIONS: Compared with labor analgesia with excellent and poor analgesia efficacy, labor analgesia with moderate analgesia efficacy has fewer cases of prolactin use, more lactation volume and time, a shorter lactation initiation time, a lower incidence of delayed onset of lactation and no effect on the LATCH score of breastfeeding.

Establishment of an animal model of sciatic nerve injury induced by local anesthetics.

Peripheral neurotoxicity injury caused by local anesthetics is a common complication of clinical anesthesia. The study of its mechanism is helpful to prevent and treat the neurotoxic injury of local anesthetics. Previous studies on peripheral neurotoxicity injury caused by local anesthetics have mainly focused on in vitro cell experiments. Due to the lack of an animal model of peripheral neurotoxicity damage caused by local anesthetics, there are few in vivo experimental studies regarding this topic. Herein, 1% ropivacaine hydrochloride was injected into the sciatic nerve by direct incision and exposure of the sciatic nerve to create a local anesthetic neurotoxic injury model. The results showed that 1% ropivacaine hydrochloride could reduce the lower limb motor score and mechanical paw withdrawal threshold in mice 48 hours after injection. Pathological sections showed that 48 hours after treatment with 1% ropivacaine hydrochloride, the sciatic nerve showed increased axonal edema and degeneration, edema between nerve fiber bundles, increased degeneration of axon and myelin sheath vacuoles, edema of nerve bundle membrane and local degeneration and necrosis, and a large number of inflammatory cells around the nerve adventitia were soaked. The above results show that under open vision, 1% ropivacaine hydrochloride can cause injury to the sciatic nerve after 48 h of treatment, which can simulate the neurotoxic damage of local anesthetics. This animal model provides a research tool for studying the mechanism of neurotoxic injury caused by local anesthetics.

Nalbuphine reduces the incidence of emergence agitation in children undergoing Adenotonsillectomy: A prospective, randomized, double-blind, multicenter study.

OBJECTIVE: To evaluate the effect of nalbuphine on emergence agitation (EA) in children undergoing adenotonsillectomy. DESIGN: Multicenter, prospective, double-blind, randomized controlled trial. SETTING: The First People's Hospital of Foshan and three other participating institutions in China, from April 2020 to December 2021. PATIENTS: Eight hundred patients, 3-9 years of age, American Society of Anesthesiologists (ASA) classification I or II, undergoing elective adenotonsillectomy were included. INTERVENTIONS: Nalbuphine (0.1 mg/kg) or saline was administered intravenously. MEASUREMENTS: The incidence of EA; the pediatric anesthesia emergence delirium (PAED) scale; and the faces, legs, activity, cry, and consolability (FLACC) scales. Extubation time, duration of post-anesthesia care unit (PACU) stay, anesthesia nurses' and parents' satisfaction, and other side effects. MAIN RESULTS: The incidence of EA in the nalbuphine group was lower than that in the saline group 30 min after extubation (10.28% vs. 28.39%, P = 0.000). In addition, the FLACC scores in the nalbuphine group were lower than those in the saline group 30 min after extubation (P < 0.05). Furthermore, the proportion of moderate-to-severe pain cases (FLACC scores >3) was significantly lower in the nalbuphine group than in the saline group (33.58% vs. 60.05%, P = 0.000). Adjusting the imbalance of postoperative pain intensity, the risk of EA was still lower in the nalbuphine group at 0 min (OR, 0.39; 95% CI, 0.26-0.60; P = 0.000), (OR, odds ratio; CI, confidence interval), 10 min (OR, 0.39; 95% CI, 0.19-0.79; P = 0.01), and 20 min (OR, 0.27; 95% CI, 0.08-0.99; P = 0.046) than in the saline group. There were no significant differences in extubation time, duration of PACU stay, nausea and vomiting, or respiratory depression between the two groups (P > 0.05). CONCLUSION: Nalbuphine reduced the incidence of EA in children after adenotonsillectomy under general anesthesia, which may be involved in both analgesic and non-analgesic pathways.

IRF-4 deficiency reduces inflammation and kidney fibrosis after folic acid-induced acute kidney injury.

The chronic phase following toxin-induced acute kidney injury (AKI) is characterized by robust inflammation and progressive kidney fibrosis. Interferon regulatory factor 4 (IRF-4) is a type of multifunctional transcription factor that has been deeply linked to inflammation and fibrotic diseases. However, the role of IRF-4 in kidney damage and renal fibrosis after toxin-induced AKI remain to be explored. In this work, we examined the effect of IRF-4 deficiency on inflammation and kidney fibrosis in an AKI-chronic kidney disease (CKD) transition model induced by folic acid (FA) injury. We showed that FA treatment resulted in severe acute tubular injury followed by inflammatory reaction and interstitial fibrosis in wild-type mice. A sharp elevation of IRF-4 levels was observed in FA-injured kidneys. IRF-4 knockout led to a substantial reduction of extracellular matrix (ECM) proteins deposition and inhibited myofibroblasts transformation in the kidneys of mice subjected to FA treatment. In addition, IRF-4 ablation impaired F4/80+ macrophages and CD3+ T lymphocytes infiltration into the FA-injured kidneys. Loss of IRF-4 reduced the production of inflammatory molecules such as CXCL16, IL-18, IL-6, and TGF-ß1 in the kidneys in response to FA stress. Following FA injury, the kidneys of IRF-4 knockout mice had fewer bone marrow-derived myofibroblasts than wild-type controls. Moreover, IRF-4 disruption inhibited macrophages to myofibroblasts differentiation in the kidneys in response to FA stimuli. In vitro, IL-4 stimulated expression of α-smooth muscle actin and ECM proteins and promoted M2 macrophages to myofibroblasts transition in mouse bone marrow-derived monocytes, which was abolished in the absence of IRF-4. Thus, we identified an important role of IRF-4 in the pathogenesis of progressive CKD following FA-induced AKI.

Community grid management is an important measure to contain the spread of novel coronavirus pneumonia (COVID-19).

The outbreak of novel coronavirus pneumonia (coronavirus disease 2019 (COVID-19)), declared as a 'global pandemic' by the World Health Organization (WHO), is a public health emergency of international concern (PHEIC). The outbreak in multiple locations shows a trend of accelerating spread around the world. China has taken a series of powerful measures to contain the spread of the novel coronavirus. In response to the COVID-19 pandemic, in addition to actively finding effective treatment drugs and developing vaccines, it is more important to identify the source of infection at the community level as soon as possible to block the transmission path of the virus to prevent the spread of the pandemic. The implementation of grid management in the community and the adoption of precise management and control measures to reduce unnecessary personnel movement can effectively reduce the risk of pandemic spread. This paper mainly describes that the grid management mode can promote the refinement and comprehensiveness of community management. As a management system with potential to improve the governance ability of community affairs, it may be helpful to strengthen the prevention and control of the epidemic in the community.

Ultrasound-guided fascia iliaca compartment block combined with general anesthesia for amputation in an acute myocardial infarction patient after percutaneous coronary intervention: A case report.

BACKGROUND: Fascia iliaca compartment block is a technique that blocks three nerves, similar to a 3-in-1 nerve block. This block provides analgesia for patients undergoing lower limb surgery, and is a simple technique that is easy to implement. Here, we report a case of fascia iliaca compartment block in a patient with myocardial infarction who underwent emergency middle thigh amputation. CASE SUMMARY: A 78-year-old female patient weighing 38 kg with gangrene and occlusive peripheral atherosclerosis of the right leg underwent an emergency middle thigh amputation. The patient had a history of hypertension, coronary heart disease, cerebral infarction, anterior wall myocardial infarction, and had recently undergone percutaneous coronary intervention consisting of coronary angiography and right coronary artery stent implantation. Considering the patient's condition, an ultrasound-guided fascia iliaca compartment block combined with general anesthesia was implemented for amputation. The fascia iliaca compartment block provided analgesia for the operation, and reduced the dosage of general anesthetics. It also alleviated adverse cardiovascular effects caused by pain stress, and ensured the safety of the patient during the perioperative period. This block also provided postoperative analgesia. The patient had a good prognosis, and was subsequently discharged from hospital. CONCLUSION: Fascia iliaca compartment block provides surgical analgesia. It also alleviates adverse cardiovascular effects, and ensures patient safety during the perioperative period.

Roles of CaMKIIß in the neurotoxicity induced by ropivacaine hydrochloride in dorsal root ganglion.

Neurotoxicity of local anesthetics is often reported in the clinic, more and more people pay attention to them. CaMKIIß, a subtype of CaMKII, is detected in the central nervous system. Previous study found that CaMKIIß mRNA are up-regulated in DRG neurons treated with ropivacaine hydrochloride, as well as inhibition of Cav3.2 and Cav3.3 expression can improve the local anesthetics neurotoxicity. In this study, we observed the effect of CaMKIIß on neurotoxicity injury induced by ropivacaine hydrochloride with DRG cell in vitro. We first constructed the pAd-shRNA-CaMKIIß-DRG to inhibit CaMKIIß mRNA expression and detected the cell viability, cell apoptosis rate, CaMKIIß, Cav3.2 and Cav3.3 expression. The results showed that ropivacaine hydrochloride caused the DRG cell injury with cell viability decreased and cell apoptosis rate increased, CaMKIIß, Cav3.2 and Cav3.3 expression up-regulated. Interestingly, inhibition of CaMKIIß expression protected the DRG cell from the neurotoxicity injury induced by ropivacaine hydrochloride, increased the cell viability and decreased the apoptosis rate, as well as inhibition of CaMKIIß expression down-regulated Cav3.2 and Cav3.3 expression. In other words, CaMKIIß is involved with the DRG injury induced by ropivacaine hydrochloride. Inhibition CaMKIIß expression improved DRG injury, increased the cell viability and decreased cell apoptosis rate.

Up-regulation of Cav3.1 expression in SH-SY5Y cells induced by lidocaine hydrochloride.

BACKGROUND: Neurotoxicity induced by the local anaesthetics has aroused concern. A previous study has shown that an overload of intracellular calcium was involved in the neurotoxic effect. Cav3.1 is one of the low-voltage-activated (LVA) calcium channels which play a key point to regulate the intracellular calcium ion level. This study aimed to investigate the changes of the Cav3.1 expression in the SH-SY5Y cells treated with lidocaine hydrochloride. METHODS: The SH-SY5Y cells were treated with different concentrations of lidocaine hydrochloride(1 mM, 5 mM and 10 mM, namely L1 group, L5 group and L10 group) and different exposure times (1 h,12 h and 24 h), respectively. Cell viability, Cav3.1 protein and mRNA expression were detected. RESULTS: The results showed that cell viability decreased and Cav3.1 mRNA and protein expression increased with the concentration (from 1 mM to 10 mM) of the lidocaine hydrochloride and exposure time (from 1 h to 24 h) to the SH-SY5Y cell line increased. CONCLUSION: Those data showed that lidocaine hydrochloride induced SH-SY5Y cell toxicity and up-regulated Cav3.1mRNA and protein expression.

In vitro neurotoxicity by ropivacaine is reduced by silencing Cav3.3 T-type calcium subunits in neonatal rat sensory neurons.

Neurotoxicity of local anaesthetics has been alerted by more and more peoples. Cav3.1 and Cav3.2 T-type calcium channels were closely related with local anaesthetics toxicity. However, the role of Cav3.3, another subtype of the T-type calcium channel, on the neurotoxicity induced by local anaesthetics remains unclear. CaMKIIγ is a kind of multifunctional kinase and associated with a variety of physiological and pathological process. T-type calcium channel is closely related with CaMKIIγ. Up-regulation CaMKIIγ can increase T-type currents at the dorsal root ganglia (DRG). On the contrary, down-regulation results in the T-type currents decrease. Is the relation between Cav3.3 T-type channel calcium and CaMKIIγ involved with the ropivacaine hydrochloride neurotoxicity? In this study, we generated pAd-Cav3.3 and pAd-shRNA adenovirus vector to up-regulate and down-regulate Cav3.3 mRNA expression of the DRG. The cells treated or untreated with ropivacaine hydrochloride (3 mM) for 4 h were used to evaluate the neurotoxicity. Cell viability, cell death rate and apoptosis rate, Cav3.3 and CaMKIIγ expression were detected with MTT method, Hoechst-PI, flow cytometry, qRT-PCR and western blotting. Results showed that the cell viability of the DRG treated with ropivacaine hydrochloride markedly decreased, death rate and apoptosis rate, Cav3.3 and CaMKIIγ mRNA and protein expression significantly increased. Cav3.3 overexpression aggravated DRG injury induced by ropivacaine hydrochloride and inhibition of Cav3.3 expression improved the cell damages. Cav3.3 can regulate CaMKIIγ mRNA and protein expression. In conclusion, Cav3.3 regulated CaMKIIγ in DRG, which was involved with the cell injury induced by ropivacaine hydrochloride.

CaMK II γ down regulation protects dorsal root ganglion neurons from ropivacaine hydrochloride neurotoxicity.

T-type calcium channels are intimately involved in the local anesthetics neurotoxicity. Does CaMKIIγ regulate T-type calcium currents in local anesthetics neurotoxicity? This study generated pAd-CaMKIIγ and pAd-shRNA adenovirus vectors to up- and down-regulate CaMKIIγ mRNA expression in dorsal root ganglion neurons (DRG). Normal DRG (Normal group), empty vector DRG (Empty vector group), pAd-CaMKIIγ DRG (pAd-CaMKIIγ group) and pAd-shRNA DRG (pAd-shRNA group) were treated or untreated with 3 mM ropivacaine hydrochloride for 4 h. Cell viability, apoptosis rate, CaMKIIγ, pCaMKIIγ, Cav3.2, and Cav3.3 expression were detected. Ultrastructural changes in DRG were observed under a transmission electron microscope. The results demonstrated that the cell viability of DRG treated with ropivacaine hydrochloride decreased markedly, the apoptosis rate, CaMKIIγ, pCaMKIIγ, Cav3.2, Cav3.3 expression increased significantly. CaMKIIγ up-regulation aggravated ropivacaine hydrochloride-induced cell damage and increased Cav3.2 and Cav3.3 expression. In conclusion, CaMKIIγ regulated Cav3.2 and Cav3.3 expression in DRG, which was involved with ropivacaine hydrochloride-induced cell injury.

Interleukin-33 signaling contributes to renal fibrosis following ischemia reperfusion.

Acute kidney injury caused by ischemia-reperfusion injury (IRI) is a major risk factor for chronic kidney disease, which is characterized by renal interstitial fibrosis. However, the molecular mechanisms underlying renal fibrosis induced by IRI are not fully understood. Our results showed that interleukin (IL)-33 was induced markedly after IRI insult, and the kidneys of mice following IRI plus IL-33 treatment presented more severe renal fibrosis compared with mice treated with IRI alone. Therefore, we investigated whether inhibition of IL-33 protects against IRI-induced renal fibrosis. Mice were administrated with soluble ST2 (sST2), a decoy receptor that neutralizes IL-33 activity, or vehicle by intraperitoneal injection for 14 days after IRI challenge. We revealed that mice treated with sST2 exhibited less severe renal dysfunction and fibrosis in response to IRI compared with vehicle-treated mice. Inhibition of IL-33 suppressed bone marrow-derived fibroblast accumulation and myofibroblast formation in the kidneys after IRI stress, which was associated with less expression of extracellular matrix proteins. Furthermore, inhibition of IL-33 also showed a significant reduction of F4/80+ macrophages and CD3+ T cells in the kidneys of mice after IRI treatment. Finally, Treatment with IL-33 inhibitor reduced proinflammatory cytokine and chemokine levels in the kidneys of mice following IRI insult. Taken together, our findings indicate that IL-33 signaling plays a critical role in the pathogenesis of IRI-induced renal fibrosis through regulating myeloid fibroblast accumulation, inflammation cell infiltration, and the expression of proinflammatory cytokines and chemokines.

Efficacy and safety of multimodal analgesic techniques for preventing chronic postsurgery pain under different surgical categories: a meta-analysis.

The purpose of this meta-analysis was to compare the efficacy and safety of regional anesthesia to manage chronic postsurgery pain. A systematic search of PubMed, EmBase, and the Cochrane Central Register of Controlled Trials was performed to identify randomized controlled trials that focused on chronic pain frequency, analgesic consumption, and adverse effects under different surgical categories. We collected 21 trials assessing 1,980 patients for our meta-analysis. The summary of relative risks (RRs) and standard mean differences (SMDs) were calculated to measure the treatment effect of regional anesthesia. Results indicated that regional anesthesia significantly reduced the frequency of postsurgery pain (RR, 0.69; 95% confidence interval [CI], 0.56-0.85; p < 0.001). The results showed significant differences in overall patient satisfaction between applications with and without regional anesthesia (SMD, 1.95; 95%CI, 0.83-3.06; p = 0.001); however in other results, there were no significant differences between the two groups. Subgroup analysis suggested that regional anesthesia treatment might differ according to country. In conclusion, our study indicated that regional anesthesia was effective and safe in reducing the frequency of postsurgery pain and improved overall patient satisfaction; however, studies on the long-term efficacy and safety of regional anesthesia are still required to further confirm these findings.

Emerging roles of GLIS3 in neonatal diabetes, type 1 and type 2 diabetes.

GLI-similar 3 (GLIS3), a member of the Krüppel-like zinc finger protein subfamily, is predominantly expressed in the pancreas, thyroid and kidney. Glis3 mRNA can be initially detected in mouse pancreas at embryonic day 11.5 and is largely restricted to ß cells, pancreatic polypeptide-expressing cells, as well as ductal cells at later stage of pancreas development. Mutations in GLIS3 cause a neonatal diabetes syndrome, characterized by neonatal diabetes, congenital hypothyroidism and polycystic kidney. Importantly, genome-wide association studies showed that variations of GLIS3 are strongly associated with both type 1 diabetes (T1D) and type 2 diabetes (T2D) in multiple populations. GLIS3 cooperates with pancreatic and duodenal homeobox 1 (PDX1), v-maf musculoaponeurotic fibrosarcoma oncogene family, protein A (MAFA), as well as neurogenic differentiation 1 (NEUROD1) and potently controls insulin gene transcription. GLIS3 also plays a role in ß cell survival and likely in insulin secretion. Any perturbation of these functions may underlie all three forms of diabetes. GLIS3, synergistically with hepatocyte nuclear factor 6 (HNF6) and forkhead box A2 (FOXA2), controls fetal islet differentiation via transactivating neurogenin 3 (NGN3) and impairment of this function leads to neonatal diabetes. In addition, GLIS3 is also required for the compensatory ß cell proliferation and mass expansion in response to insulin resistance, which if disrupted may predispose to T2D. The increasing understanding of the mechanisms of GLIS3 in ß cell development, survival and function maintenance will provide new insights into disease pathogenesis and potential therapeutic target identification to combat diabetes.

One cell model establishment to inhibit CaMKIIγ mRNA expression in the dorsal root ganglion neuron by RNA interfere.

CaMKIIγ in dorsal root ganglion neurons is closely related to the neuropathic pain, neuron injury induced by local anesthetics. To get great insight into the function of CaMKIIγ in dorsal root ganglion neurons, we need one cell model to specially inhibit the CaMKIIγ mRNA expression. The present study was aimed to establish one cell model to specially inhibit the CaMKIIγ mRNA expression. We designed the CaMKIIγ shRNA sequence and connected with pYr-1.1 plasmid. The ligation product of the CaMKIIγshRNA and pYr-1.1 plasmid was recombined with pAd/PL-DEST vector into pAD-CaMKIIγ-shRNA. adenovirus vector. pAD-CaMKIIγ-shRNA. adenovirus vector infected the dorsal root ganglion neuron to inhibit the CaMKIIγ mRNA expression in vitro. The pAD-CaMKIIγ-shRNA adenovirus vector was verified to be correct by the digestion, sequence. And pAD-CaMKIIγ-shRNA. adenovirus vector can infect the DRG cells to inhibit the CaMKIIγ mRNA or protein expression by the real-time polymerase chain reaction (PCR) or western blotting. Those results showed that we successfully constructed one adenovirus vector that can infect the dorsal root ganglion neuron to inhibit the CaMKIIγ mRNA and protein expression. That will supply with one cell model for the CaMKIIγ function study.