Design of a miniaturized dual circularly polarized implantable antenna by using characteristic mode method.

The characteristic mode method is used to design a miniaturized dual-band dual circularly polarized (CP) implantable antenna operating in ISM bands. The miniaturization and dual-band characteristics are gained by using the slotting method and by inserting a short-circuit probe between the radiation patch and the ground plane. We use the characteristic mode method to study the current distribution of circular radiation patches with T-shaped slots in different modes. After opening a cross-shaped slot at the center of the radiation patch and the ground plane, we obtained two orthogonal modes with equal amplitude and phase difference of 90° in two operating frequency bands, ultimately achieving CP characteristics of the antenna. Its overall size is only π ×(0.014 λ 0)2 × 0.0027 λ 0, smaller than other CP implantable antennas with similar performances, and it has satisfactory radiation efficiency and gain characteristics. Measurements show that it can operate in the ISM bands of 0.9 and 2.4 GHz with an effective 3 dB axial ratio bandwidth greater than 220 MHz (0.87 to 1.09 GHz, 22.45%) and 230 MHz (2.31 to 2.54 GHz, 9.48%), and its peak gain is - 29.5 dBi and - 19.2 dBi, respectively. And, this design complies with IEEE safety guidelines.

A Miniaturized Dual-Band Circularly Polarized Implantable Antenna for Use in Hemodialysis.

Hemodialysis is achieved by implanting a smart arteriovenous graft (AVG) to build a vascular pathway, but reliability and stability in data transmission cannot be guaranteed. To address this issue, a miniaturized dual-band circularly polarized implantable antenna operating at 1.4 GHz (for energy transmission) and 2.45 GHz (for wireless telemetry), implanted in a wireless arteriovenous graft monitoring device (WAGMD), has been designed. The antenna design incorporates a rectangular serpentine structure on the radiation surface to reduce its volume to 9.144 mm3. Furthermore, matching rectangular slots on the radiation surface and the ground plane enhance the antenna's circular polarization performance. The simulated effective 3 dB axial ratio (AR) bandwidths are 11.43% (1.4 GHz) and 12.65% (2.45 GHz). The simulated peak gains of the antenna are -19.55 dBi and -22.85 dBi at 1.4 GHz and 2.45 GHz, respectively. The designed antenna is implanted in a WAGMD both in the simulation and the experiment. The performance of the system is simulated in homogeneous human tissue models of skin, fat, and muscle layers, as well as a realistic adult male forearm model. The measurement results in a minced pork environment align closely with the simulation results.

EAF2 Downregulation Recruits Tumor-associated Macrophages in Prostate Cancer through Upregulation of MIF.

BACKGROUND: The role of tumor inflammatory microenvironment in the advancement of cancer, particularly prostate cancer, is widely acknowledged. ELL-associated factor 2 (EAF2), a tumor suppressor that has been identified in the prostate, is often downregulated in prostate cancer. Earlier investigations have shown that mice with EAF2 gene knockout exhibited a substantial infiltration of inflammatory cells into the prostatic stroma. METHODS: A cohort comprising 38 patients who had been diagnosed with prostate cancer and subsequently undergone radical prostatectomy (RP) was selected. These patients were pathologically graded according to the Gleason scoring system and divided into two groups. The purpose of this selection was to investigate the potential correlation between EAF2 and CD163 using immunohistochemistry (IHC) staining. Additionally, in vitro experimentation was conducted to verify the relationship between EAF2 expression, macrophage migration and polarization. RESULTS: Our study demonstrated that in specimens of human prostate cancer, the expression of EAF2 was notably downregulated, and this decrease was inversely associated with the number of CD163-positive macrophages that infiltrated the cancerous tissue. Cell co-culture experiments revealed that the chemotactic effect of tumor cells towards macrophages was intensified and that macrophages differentiated into tumor-associated macrophages (TAMs) when EAF2 was knocked out. Additionally, the application of cytokine protein microarray showed that the expression of chemokine macrophage migration inhibitory factor (MIF) increased after EAF2 knockout. CONCLUSIONS: Our findings suggested that EAF2 was involved in the infiltration of CD163-positive macrophages in prostate cancer via MIF.

Design of a Compact Circularly Polarized Implantable Antenna for Capsule Endoscopy Systems.

This research proposes a miniature circular polarization antenna used in a wireless capsule endoscopy system at 2.45 GHz for industrial, scientific, and medical bands. We propose a method of cutting a chamfer rectangular slot on a circular radiation patch and introducing a curved radiation structure into the centerline position of the chamfer rectangular slot, while a short-circuit probe is added to achieve miniaturization. Therefore, we significantly reduced the size of the antenna and made it exhibit circularly polarized radiation characteristics. A cross-slot is cut in the GND to enable the antenna to better cover the operating band while being able to meet the complex human environment. The effective axis ratio bandwidth is 120 MHz (2.38-2.50 GHz). Its size is π × 0.032λ02 × 0.007λ0 (where λ0 is the free-space wavelength of at 2.4 GHz). In addition, the effect of different organs such as muscle, stomach, small intestine, and big intestine on the antenna when it was embedded into the wireless capsule endoscopy (WCE) system was further discussed, and the results proved that the WCE system has better robustness in different organs. The antenna's specific absorption rate can follow the IEEE Standard Safety Guidelines (IEEE C95.1-1999). A prototype is fabricated and measured. The experimental results are consistent with the simulation results.

Simultaneous thulium laser resection of the prostate and transperineal prostate biopsy in clinically diagnosed metastatic prostate cancer with bladder outlet obstruction.

Metastatic prostate cancer (mPCa) patients complicated with bladder outlet obstruction (BOO) are often referred to a urologist. Androgen deprivation therapy (ADT) combined with indwelling catheter usually be the initial management. To retrospectively analysis the safety and efficacy of simultaneous thulium laser resection of the prostate (TmLRP) and transperineal prostate biopsy in metastatic prostate cancer with bladder outlet obstruction. From January 2016 to December 2021, 67 clinically diagnosed mPCa with BOO patients were included in this study. All patients were preoperatively assessed with international prostate symptom score (IPSS), QoL, serum prostate-specific antigen (PSA), prostate volume evaluation by transrectal ultrasound, postvoid residual urine volume (PVR), and maximum flow rate (Qmax). Preoperative and perioperative parameters at 1-, 3-, and 6-month follow-up were also evaluated. All complications were recorded. Simultaneous TmLRP and transperineal prostate biopsy had obvious advantages for clinically diagnosed mPCa patients with BOO, including short overall operation time (52 ± 23.3 min), little hemoglobin decrease (0.6 ± 0.7 g/l), and short hospital stay (average 3.8 days). In addition, simultaneous TmLRP and transperineal prostate biopsy also brought them significant improvement on IPSS, QoL score, Qmax, and PVR volume (P < 0.001) at 1-, 3-, and 6-month follow-up after operation compared to preoperative parameters. Complications were in a low incidence. Simultaneous TmLRP and transperineal prostate biopsy is a bloodless operation with immediate effect and little perioperative complication. Importantly, it is a promising technology in the diagnosis and treatment of clinically diagnosed mPCa patients with BOO.

Rapamycin and Low-dose IL-2 Mediate an Immunosuppressive Microenvironment to Inhibit Benign Prostatic Hyperplasia.

Benign prostatic hyperplasia (BPH) is a condition that becomes more common with age and manifests itself primarily as the expansion of the prostate and surrounding tissues. However, to date, the etiology of BPH remains unclear. In this respect, we performed single-cell RNA sequencing of prostate transition zone tissues from elderly individuals with different prostate volumes to reveal their distinct tissue microenvironment. Ultimately, we demonstrated that a reduced Treg/CD4+ T-cell ratio in the large-volume prostate and a relatively activated immune microenvironment were present, characterized partially by increased expression levels of granzymes, which may promote vascular growth and profibrotic processes and further exacerbate BPH progression. Consistently, we observed that the prostate gland of patients taking immunosuppressive drugs usually remained at a smaller volume. Furthermore, in mouse models, we confirmed that both suppression of the immune system with rapamycin and induction of Treg proliferation with low doses of IL-2 therapy indeed prevented the progression of BPH. Taken together, our findings suggest that an activated immune microenvironment is necessary for prostate volume growth and that Tregs can reverse this immune activation state, thereby inhibiting the progression of BPH.

Targeting ADT-Induced Activation of the E3 Ubiquitin Ligase Siah2 to Delay the Occurrence of Castration-Resistant Prostate Cancer.

Siah2 is an E3 ubiquitin ligase that targets androgen receptor (AR) and plays an important role in the development of castration-resistant prostate cancer (CRPC). However, the regulation of Siah2 in prostate cancer (PCa) is largely unknown. In this study, we used AR-dependent and -independent cells lines to investigate the cellular roles of AR and androgen deprivation therapy (ADT) on Siah2 protein levels and E3 ligase activity using Western blotting and co-immunoprecipitation. We also validated our findings using patient samples taken before and after ADT. Finally, we used xenograft tumor models to test the effects of ADT combined with vitamin K3 (Vit K3) on tumor growth in vivo. Our results showed that AR stabilizes Siah2 protein by attenuating its self-ubiquitination and auto-degradation, likely by blocking its E3 ubiquitin ligase activity. Conversely, ADT decreased Siah2 protein expression but enhanced its E3 ligase activity in PCa cells. Notably, the findings that ADT decreasing Siah2 protein expression were verified in a series of paired PCa samples from the same patient. Additionally, we found that ADT-induced Siah2 activation could be abolished by Vit K3. Strikingly, ADT combined with Vit K3 treatment delayed the occurrence of CRPC and dramatically inhibited the growth of tumor xenografts compared with ADT treatment alone. AR is an inhibitor of Siah2 in PCa, and ADT leads to the continuous activation of Siah2, which may contribute to CRPC. Finally, ADT+Vit K3 may be a potential approach to delay the occurrence of CRPC.

Upregulation of miR-202-5p promotes cell apoptosis and suppresses cell viability of hypoxia-induced myocardial H9c2 cells by targeting SOX6 to inhibit the activation of the PI3K/AKT/FOXO3a pathway.

This study aimed to investigate the potential role of microRNA-202-5p (miR-202-5p) in regulating myocardial ischemia-caused injury and to explore the underlying mechanisms. Rat embryonic ventricular cardiomyocyte-derived H9c2 cells were treated with hypoxia to generate an in vitro myocardial ischemia model, followed by the transfection with a miR-202-5p mimic and inhibitor. Subsequently, the effects of miR-202-5p on cell viability, apoptosis, migration, and invasion were analyzed. A luciferase reporter assay was used to identify the target gene of miR-202-5p. Besides, the regulatory relationship between miR-202-5p and the PI3K/AKT/FOXO3a pathway was investigated in hypoxia-induced H9c2 cells. Compared to normal H9c2 cells, the hypoxia treatment resulted in a significant damage to H9c2 cells, thereby decreasing the cell viability, migration, and invasion ability and inducing the cell apoptosis. miR-202-5p was significantly upregulated in hypoxia-induced H9c2 cells. After cell transfection, the suppression of miR-202-5p significantly alleviated the hypoxia-induced damage in H9c2 cells through the suppression of cell apoptosis and the promotion of cell viability, migration, and invasion ability. SRY-box 6 (SOX6) was found to be a direct target of miR-202-5p. The knockdown of SOX6 significantly aggravated the hypoxia-induced myocardial damage to H9c2 cells, which was alleviated after the inhibition of miR-202-5p expression. Besides, miR-202-5p suppression resulted in the activation of the PI3K/AKT/FOXO3a pathway in H9c2 cells. The data presented in this study revealed that miR-202-5p was upregulated in H9c2 cells during myocardial ischemia. The overexpressed miR-202-5p may aggravate the myocardial ischemia-caused injury by downregulating SOX6 to suppress the activation of the PI3K/AKT/FOXO3a pathway. Thus, miR-202-5p may serve as a potential target for the clinical treatment of myocardial ischemia.

Danshensu protects against ischemia/reperfusion injury and inhibits the apoptosis of H9c2 cells by reducing the calcium overload through the p-JNK-NF-κB-TRPC6 pathway.

Ischemia-reperfusion (I/R) plays an important role in myocardial injury. In the present study, we aimed to examine the protective effects of Danshensu (DSS) against I/R injury and to elucidate the underlying mechanisms. For this purpose, H9c2 cells were cultured in hypoxic solution in a hypoxic incubator for 2 h, and then cultured in a high oxygen incubator for various periods of time and pre-treated with or without DSS, ammonium pyrrolidine dithiocarbamate (PDTC) or SP600125 [a c-Jun N-terminal kinase (JNK) inhibitor]. Cell apoptosis and cytosolic free Ca2+ ([Ca2+]i) levels were analyzed by flow cytometry. The protein expression levels of JNK, phosphorylated (p-)JNK, nuclear factor-κB (NF-κB) and transient receptor potential cation channel, subfamily C, member 6 (TRPC6) were measured by western blot analysis. The mRNA expression levels of JNK were measured by RT-qPCR. The results revealed that TRPC6 protein expression, the cell apoptotic rate and the [Ca2+]i levels increased in a time-dependent manner in the H9c2 cells following the induction of I/R injury. The apoptotic rate and TRPC6 protein expression decreased when the cells were treated with DSS prior to the induction of I/R injury. The knockdown of JNK expression by siRNA decreased the p-JNK and TRPC6 protein expression levels in the H9c2 cells subjected to I/R injury. The protein expression levels of p-JNK and NF-κB in the nucleus increased significantly when the H9c2 cells were subjected to I/R injury, whereas NF-κB expression in the cytoplasm decreased in a time­dependent manner. However, p-JNK, NF-κB and TRPC6 protein expression, the [Ca2+]i level and cell apoptosis decreased when the H9c2 cells were pre-treated with DSS or SP600125. Therefore, our data suggest that DSS prevents myocardial I/R injury by inhibiting p-JNK activation and NF-κB translocation, which potentially upregulate TRPC6 expression, increase the [Ca2+]i level, and result in the apoptosis of H9c2 cells.

[The safety and outcome of patients with acute myocardial infarction transferred for primary angioplasty].

OBJECTIVE: To evaluate the safety and outcome of patients with acute myocardial infarction (AMI) transferred for primary percutaneous coronary intervention (PCI). METHODS: Data from patients with ST elevation AMI urgently transferred from first admitted hospitals to our cath-lab to receive primary PCI were analyzed. According to time intervals from symptom onset to transfer, the patients were divided into early transfer (< 6 h, n = 26), delayed transfer (6 - 24 h, n = 39) and late transfer (24 h to 1 week, n = 18) group. The major cardiac events during transfer periods and one month after PCI were obtained and echocardiogram and left ventricular systolic functions were compared among groups. RESULTS: There was no serious cardiac event during transfer period and all 83 patients received primary PCI with a mean transfer-to-balloon time about 180 minutes. Success rate of PCI was 92.3% in early transfer group, 89.7% in delayed transfer group, and 94.4% in late transfer group (P > 0.05). At one month follow-up after PCI, 0, 10.3% and 16.7% of patients developed heart failure in early, delayed transfer and late transfer group respectively (P > 0.05 vs. early), the LVEF of early transfer group (53.2% +/- 9.7%) was also significantly higher than delayed transfer group (48.6% +/- 8.2%, P < 0.05) and late transfer group (43.1% +/- 10.3%, P < 0.01). CONCLUSIONS: Transfer patients with AMI for primary PCI is safe in the observed time intervals during acute phase. Early transferred patients are associated with better outcome at 1 month post PCI compared to delayed and late transferred AMI patients.