W-Band Beam-Tilted H-Plane Horn Array Antenna with Wideband Integrated Waveguide Feed Network Based on MMPTE.

A W-band H-plane horn array antenna with tilted radiation beam based on waveguide structure is proposed in this paper. The designed antenna array consists of four H-plane antenna elements and a broadband feed network. The distribution of excitations is determined by the theory of maximum power transmission efficiency (MMPTE). A multiple branch coupler, two T-junctions and three fixed phase shifters are employed to construct the feed network, which can generate the required amplitude and phase in broadband frequency range from 80 GHz to 100 GHz. The computer numerical control (CNC) milling machines technology is employed to machine the feed network and antenna. All measured and simulated results are in good agreement, which verify the feasibility of the theory of MMPTE to generate a radiation beam directed to any angle from -35° to 35° with suitable excitation provided by the proposed feed network in this paper.

Bioinformatics analysis identifies potential ferroptosis key genes in the pathogenesis of diabetic peripheral neuropathy.

Background: Diabetic peripheral neuropathy (DPN) is a serious complication in Diabetes Mellitus (DM) patients and the underlying mechanism is yet unclear. Ferroptosis has been recently intensively researched as a key process in the pathogenesis of diabetes but there yet has been no related bioinformatics-based studies in the context of DPN. Methods: We used data mining and data analysis techniques to screen differentially expressed genes (DEGs) and immune cell content in patients with DPN, DM patients and healthy participants (dataset GSE95849). These DEGs were then intersected with the ferroptosis dataset (FerrDb) to obtain ferroptosis DEGs and the associated key molecules and miRNAs interactions were predicted. Results: A total of 33 ferroptosis DEGs were obtained. Functional pathway enrichment analysis revealed 127 significantly related biological processes, 10 cellular components, 3 molecular functions and 30 KEGG signal pathways. The biological processes that were significantly enriched were in response to extracellular stimulus and oxidative stress. Key modules constructed by the protein-protein interaction network analysis led to the confirmation of the following genes of interest: DCAF7, GABARAPL1, ACSL4, SESN2 and RB1. Further miRNA interaction prediction revealed the possible involvement of miRNAs such as miR108b-8p, miR34a-5p, mir15b-5p, miR-5838-5p, miR-192-5p, miR-222-3p and miR-23c. Immune-environment content of samples between DM and DPN patients revealed significant difference in the levels of endothelial cells and fibroblasts, which further speculates their possible involvement in the pathogenesis of DPN. Conclusion: Our findings could provide insight for investigations about the role of ferroptosis in the development of DPN.

Effects of propofol on sleep architecture and sleep-wake systems in rats.

Previous studies have shown that the synchronization of electroencephalogram (EEG) signals is found during propofol-induced general anesthesia, which is similar to that of slow-wave sleep (SWS). However, a complete understanding is lacking in terms of the characteristics of EEG changes in rats after propofol administration and whether propofol acts through natural sleep circuits. Here, we examined the characteristics of EEG patterns induced by intraperitoneal injection of propofol in rats. We found that high (10 mg/kg) and medium (5 mg/kg) doses of propofol induced a cortical EEG of low-frequency, high-amplitude activity with rare electromyographic activity and markedly shortened sleep latency. The high dose of propofol increased deep slow-wave sleep (SWS2) to 4 h, as well as the number of large SWS2 bouts (>480 s), their mean duration and the peak of the power density curve in the delta range of 0.75-3.25 Hz. After the medium dose of propofol, the total number of wakefulness, light slow-wave sleep (SWS1) and SWS2 episodes increased, whereas the mean duration of wakefulness decreased. The high dose of propofol significantly increased c-fos expression in the ventrolateral preoptic nucleus (VLPO) sleep center and decreased the number of c-fos-immunoreactive neurons in wake-related systems including the tuberomammillary nucleus (TMN), perifornical nucleus (PeF), lateral hypothalamic nucleus (LH), ventrolateral periaqueductal gray (vPAG) and supramammillary region (SuM). These results indicated that the high dose of propofol produced high-quality sleep by increasing SWS2, whereas the medium dose produced fragmented and low-quality sleep by disrupting the continuity of wakefulness. Furthermore, sleep-promoting effects of propofol are correlated with activation of the VLPO cluster and inhibition of the TMN, PeF, LH, vPAG and SuM.

Chinese Association for the Study of Pain: Experts consensus on ultrasound-guided injections for the treatment of spinal pain in China (2020 edition).

Spinal pain (SP) is a common condition that has a major negative impact on a patient's quality of life. Recent developments in ultrasound-guided injections for the treatment of SP are increasingly being used in clinical practice. This clinical expert consensus describes the purpose, significance, implementation methods, indications, contraindications, and techniques of ultrasound-guided injections. This consensus offers a practical reference point for physicians to implement successfully ultrasound-guided injections in the treatment of chronic SP.

Association of genetic polymorphisms in STAT1 gene with increased risk of hepatocellular carcinoma.

OBJECTIVE: Although signal transducer and activator of transcription 1 (STAT1), a transcription factor, plays a critical role in carcinogenesis and has been implicated as a tumor suppressor, few studies have investigated the associations between polymorphisms of this gene and the risk of cancer development. The aim of this study was to examine whether STAT1 gene polymorphisms are associated with the risk of hepatocellular carcinoma (HCC). METHODS: Ten single nucleotide polymorphisms in the STAT1 gene were genotyped by TaqMan assays in 469 HCC cases and 558 age-, sex- and HBsAg-matched controls in a Chinese population. RESULTS: Minor allele homozygous genotypes at rs867637 (9,046 bp 3' of STP A>G), rs3771300 (IVS24-153T>G), and rs2280235 (IVS20-103G>A), compared with their homozygote genotypes of common alleles, were associated with 1.6- (95% CI 1.1-2.3), 1.6- (95% CI 1.1-2.4), and 1.4-fold (95% CI 0.95-1.9) increased risk of HCC, respectively. The GGA haplotype, comprised of risk alleles at rs867637, rs3771300 and rs2280235, conferred a 1.2-fold (95% CI 1.0-1.5) increased risk of HCC, as compared to the most common haplotype of ATG. Diplotype GGA/GGA conferred a 1.6-fold (95% CI 1.0-2.5) increased risk of HCC compared with diplotype ATG/ATG. CONCLUSION: Our results demonstrate for the first time that polymorphisms in the STAT1 gene are associated with HCC susceptibility.

DJ-1 plays a neuroprotective role in SH-SY5Y cells by modulating Nrf2 signaling in response to lidocaine-mediated oxidative stress and apoptosis.

To investigate the effects of DJ-1 on lidocaine-induced cytotoxicity in neurons and the link with Nrf2 signaling, SH-SY5Y cells were treated with 1, 4, 8, and 16 mM lidocaine. Cell viability was measured by MTT assay, and apoptosis was measured by flow cytometry analysis. The mitochondrial membrane potential, reactive oxygen species (ROS) levels, lipid peroxidation (MDA), and GSH/GSSG ratio were determined with specific kits. Expression of DJ-1, Nrf2, and Nrf2 downstream signaling proteins (glutathione peroxidase [GPx], heme oxygenase-1 [HO-1], catalase [CAT], and glutathione reductase [GR]), was determined by western blot and qRT-PCR. The cell viability was dramatically decreased, while levels of apoptosis, ROS and Cys106-oxidized DJ-1 were significantly enhanced following treatment with lidocaine (concentration 4-16 mM), and increases were observed in a dose-dependent manner. After treatment with 8 mM lidocaine, DJ-1, and nuclear Nrf2, as well as antioxidative stress-related proteins, GPx, GR, HO-1, and CAT, were all significantly inhibited. Overexpression of DJ-1 suppressed lidocaine-induced apoptosis and oxidative stress in SH-SY5Y cells and activated Nrf2 signalling at the same time, and these effects were reversed by the inhibition of Nrf2. DJ-1 could protect SH-SY5Y cells from lidocaine-induced apoptosis through inhibition of oxidative stress via Nrf2 signaling.

[Expression of metabotropic glutamate receptor 5 in spinal cord of morphine tolerant rats].

OBJECTIVE: To investigate the expression of metabotropic glutamate receptor 5 (mGluRS) in spinal cord of morphine tolerant rats and understand the influence of mGluR5 antagonist MPEP upon the expression of mGluRS. METHODS: Male Sprague-Dawley rats were randomly divided into four groups with 8 rats each:control group (NS), morphine group, morphine plus MPEP group and MPEP group. A morphine tolerance model of rat was established by repeated administration of 10 microg morphine intrathecally twice daily for 7 days. The effects of morphine co-administrated with MPEP upon the thermal pain threshold were examined by tail flick test. Tail flick latency (TFL) was measured at 30 min pre- and postdosing. MPE% (percentage of maximal possible effect) was calculated by the equation: MPE (%) = [(test response time-basal response time)/(cut-off time-basal response time)] x 100%. The rats were sacrificed and L4-5 spinal cord tissue was removed. The expression of mGluR5 in every group was examined by immunofluorescence and Western blot. RESULTS: MPE% of morphine group decreased gradually after chronic administration of morphine intrathecally. There was no significant difference between morphine group and control group at Day 7 (P > 0.05). Morphine plus MPEP group had significant analgesic effect as compared with morphine group at Day 7 (P < 0.05). The expression of mGluR5 was up-regulated in the dorsal horn of spinal cord in morphine tolerant rats. The protein level of mGluRS in morphine plus MPEP group was lower than that in morphine group (P < 0.05), but higher than control group (P < 0.05). CONCLUSION: The mGluR5 antagonist MPEP can prevent the development of morphine tolerance. The expression of mGluR5 protein increases in the spinal cord of morphine tolerant rats. MPEP plays its role in morphine tolerance by partly inhibiting the expression of mGluRS.

The differences between venous air embolism and fat embolism in routine intraoperative monitoring methods, transesophageal echocardiography, and fatal volume in pigs.

BACKGROUND: Venous air embolism (VAE) or fat embolism (FE) may occur in similar clinical settings such as after multiple injuries or total hip replacement. We designed this study to observe the differences between VAE and FE in routine intraoperative monitoring methods, transesophageal echocardiography (TEE), and fatal volume in pigs. METHODS: Sixteen domestic pigs were randomly assigned to either a fat group (n = 8) or an air group (n = 8). Each animal was injected with a series of volumes of air or fat. TEE and routine intraoperative monitoring were used during the experiment. The echogenic pattern of air or fat emboli were recorded and was graded (grade 0, no emboli; grade 1, a few fine emboli; grade 2, embolic masses less than 5 mm in diameter and the right atrium opacified with echogenic materials; grade 3, fine emboli mixed with large embolic masses greater than 5 mm in diameter or serpentine emboli). Precordial auscultation was performed before and after each injection of air or fat. The fatal volumes of air and fat were recorded. RESULTS: No echogenic pattern grade 3 on TEE in the fat group was observed even fatal volume of fat was injected, whereas echogenic pattern grade 3 was found in all pigs in the air group when > or = 0.5 mg/kg of air was injected (0/8 vs. 8/8, p < 0.01). Paradoxical embolism and cutaneous petechiae was more common in the fat group than in the air group (8/8 vs. 1/8, 6/8 vs. 0/8, p < 0.05). "Bubble-like" sounds, "drum-like" murmurs, and "mill-wheel" murmurs were only heard in the air group but not in the fat group (8/8 vs. 0/8, p < 0.01). Fatal volume of air was much higher than that of fat (4 mL/kg +/- 0.76 mL/kg vs. 0.24 mL/kg +/- 0.05 mL/kg, p < 0.01). CONCLUSIONS: Large extensive echogenic masses on TEE, "bubble-like" sounds, "drum-like" murmurs, and "mill-wheel" murmurs were more likely associated with VAE. All of fat emboli were fine on TEE. Paradoxical embolism and cutaneous petechiae were more common in FE. Fatal volume of fat is lower than that of air.

[Association of TP53 gene polymorphisms with genetic susceptibility to liver metastases of colorectal cancer].

OBJECTIVE: To investigate the possible association between the single nucleotide polymorphisms (SNPs) (C-8343G, C-1863T and R72P) in TP53 gene and susceptibility to liver metastases of colorectal cancer (CRC) in a Chinese population. METHODS: The genotypes of each SNP in TP53 gene were determined by either TaqMan assays or PCR-based restriction fragment length polymorphism (RFLP) method in 121 colorectal cancer patients with liver metastases and sex-, age-matched 280 cases with nonmetastatic CRC as a control. Immunohistochemical staining for P53 was performed on paraffin-embedded sections. Odds ratios (ORs) for colorectal liver metastases and 95% confidence intervals (CIs) from unconditional logistic regression models were used to evaluate relative risks. RESULTS: No significant association of C-8343G or C-1863T with colorectal liver metastases risk was observed. However, the R allele of the TP53 R72P polymorphism was more frequently found in metastatic cases than in nonmetastatic cases (P= 0.037). When compared with PP homozygotes, the ORs of metastases for RP heterozygotes was 2.21 (95% CI: 1.13-4.33), for RR homozygotes was 2.26 (95% CI: 1.03-4.94), and for carriers of the 72R allele (RP or RR genotype) was 2.22 (95% CI: 1.16-4.26). Stratified analysis indicated that carrying the 72R allele had a more pronounced increase in colorectal liver metastases risk among patients with positive P53 expression tumors (OR= 3.28, 95% CI: 1.21-8.88), whereas no significantly increased metastases risk was found in patients with negative P53 expression tumors (OR= 1.37, 95% CI: 0.52-3.62). CONCLUSION: The R allele of the TP53 R72P polymorphism may contribute to the etiology of liver metastases in CRC patients, particularly among those with positive P53 expression tumors. Both TP53 C-8343G and C-1863T may be not associated with colorectal liver metastases risk.

Association of p53 codon 72 polymorphism with liver metastases of colorectal cancers positive for p53 overexpression.

OBJECTIVE: To evaluate the association between p53 codon 72 polymorphism (R72P) and the risk of colorectal liver metastases. METHODS: The p53 R72P genotype was identified by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method in 78 consecutive colorectal cancer patients with liver metastases and 214 age- and sex-matched cases with nonmetastatic colorectal cancer. RESULTS: The R allele of the p53 R72P polymorphism was more frequently found in metastatic cases than in nonmetastatic cases (P=0.075). Carriers of the 72R allele had a 2.25-fold (95% CI (confidence interval)=1.05 to approximately 4.83) increased risk of liver metastases. On the stratification analysis, 72R-carrying genotype conferred a 3.46-fold (95% CI=1.02 to approximately 11.72) and a 1.05-fold (95% CI=0.36 to approximately 3.08) increased risk of liver metastases for p53 overexpression-positive and negative colorectal cancers, respectively. CONCLUSION: These results demonstrate for the first time that the 72R allele of the p53 polymorphism has an increased risk for liver metastases in colorectal cancers positive for p53 overexpression.

Association of the TP53 codon 72 polymorphism with colorectal cancer in a Chinese population.

A TP53 gene polymorphism, resulting in an arginine (R) to proline (P) at codon 72 (TP53 R72P), has been associated with the susceptibility to various cancers. To better understand the role of this polymorphism in colorectal cancer etiology, we examined the association between TP53 R72P and colorectal cancer risk in 345 patients with colorectal cancer and 670 controls in a Chinese population. We observed that subjects with RP and PP genotypes had a 1.60-fold and a 2.37-fold increased risk for colorectal cancer, respectively. The 72P allele conferred a more pronounced increase in colorectal cancer risk among alcohol consumers (heterozygotes: OR = 3.01; homozygotes: OR = 4.71). The TP53 R72P polymorphism was not linked to tumor location, histologic grade, lymph node metastases, Dukes stage, p53 positivity, or age at diagnosis, but to tumor size. We conclude that the TP53 R72P polymorphism may contribute to the etiology of colorectal cancer in the Chinese population, particularly among alcohol consumers.

[TP53 gene polymorphisms and colorectal cancer risk in Chinese population].

OBJECTIVE: To investigate the association between the single nucleotide polymorphisms (SNPs) in TP53 gene and susceptibility to colorectal cancer (CRC) in Chinese population. METHODS: Peripheral blood samples were collected and white cell genomic DNA was extracted from 345 CRC patients, 198 males and 1447 females, aged (58.7 +/- 13.5), and 670 sex, age, smoking and drinking situations-matched controls in Ningbo city, Zhejiang province The genotypes of the SNPs of C-8343G, C-1863T, and R72P in TP53 gene were determined by either TaqMan assays or PCR-based restriction fragment length polymorphism method. Unconditional logistic regression was used to calculate the odds ratio (OR) for CRC after adjustment of the covariates, such as sex, age, cigarette smoking, alcohol drinking, body mass index and first-degree family history of CRC, and 95% confidence intervals (CI) so as to evaluate relative risk. RESULTS: There were not significant differences in the above mentioned covariates between these 2 groups. No significant association of C-8343G or C-1863T polymorphism with CRC risk was observed (both P > 0.05). The CRC risk of the 72P genotype was 50.3%, 1.53 times that of the 72R genotype (39.6%) (95% CI = 1.27 - 1.85, P < 0.01). The CRC risk of the RP heterozygotes was 1.60 times that of the RP homozygote (95% CI = 1.17 - 2.18, P < 0.01), and the CRC risk of the PP homozygotes was 2.37 times that of the RP heterozygotes (95% CI = 1.61 - 3.47, P < 0.01). A dose-response relationship was shown (P < 0.01). Stratified analysis indicated that the 72P allele conferred a more pronounced increase in CRC risk among the alcohol consumers: the CRC risk was 3.01 times for the RP heterozygotes (95% CI = 1.48 - 6.12), and 4.71 times for the PP homozygotes (95% CI = 1.90 - 11.68). CONCLUSION: TP53 C-8343G and C-1863T polymorphisms are not associated with CRC risk. R72P polymorphism contributes to the etiology of CRC in the Chinese population, particularly among the alcohol consumers.

Rac2 deficiency attenuates CCl4-induced liver injury through suppressing inflammation and oxidative stress.

Oxidative stress is a leading cause to liver injury. Rac2 is a Ras-associated guanosine triphosphatase, an important molecule modulating a large number of cells and involved in the regulation of reactive oxygen species (ROS). For the study described here, we supposed that Rac2 knockout protects mice against CCl4-induced acute liver injury. We found that Rac2 expressed highly in CCl4-induced liver tissues. CCl4-treated Rac2 knockout (Rac2-/-) mice had reduced CD24 levels and steatosis. In addition, CCl4-induced high expression of pro-inflammatory cytokines and chemokine were reversed by Rac2 deficiency compared to CCl4-treated wild type (WT) mice. We also found that fibrosis-related signals of MMP-9, MMP-2 and TGF-ß1 were also down-regulated in Rac2 knockout mice induced by CCl4. Significantly, oxidative stress induced by CCl4 was also suppressed owing to the lack of Rac2, evidenced by enhanced superoxide dismutase (SOD) activity, and reduced malondialdehyde (MDA) levels, superoxide radical, H2O2, xanthine oxidase (XO), xanthine dehydrogenase (XDH) and XO/XDH ratio. Moreover, c-Jun N-terminal protein kinase mitogen-activated protein kinases (JNK MAPK) was activated by CCl4, which was reversed in the liver of Rac2-/- mice through western blot and immunohistochemical analysis. In vitro, endotoxin (LPS) was treated to hepatocytes isolated from WT mice and Rac2-/- mice. The data further confirmed the role of Rac2 deficiency suppressed pro-inflammatory cytokines and chemokine, as well as fibrosis-related signals. Of note, production of ROS induced by LPS was reduced in Rac2-/- cells, accompanied with enhanced SOD1, SOD2 and reduced XO and phosphorylated-JNK expressions. Our results indicated that Rac2 played an essential role in acute liver injury induced by CCl4, providing the compelling information of the effects of Rac2 on liver injury, and revealing a novel regulatory mechanism for acute liver injury.