113Gbps rainbow visible light laser communication system based on 10λ laser WDM emitting module in fiber-free space-fiber link.

With the advent of the sixth-generation mobile communication standard (6 G), the visible light communication (VLC) technology based on wavelength division multiplexing (WDM) technology can effectively solve the problem of shortage of spectrum resources and insufficient channel capacity. This paper introduces one of our technical achievements, namely the construction of a near-real-time visible light laser communication (VLLC) system based on WDM, which includes a self-designed 10-λ fully-packaged visible light laser emission module, 1 m multimode fiber - 0.175 m free space - 1 m multimode fiber optical transmission link, and receiver array. In the transmitter system, we adopt adaptive discrete multitone (DMT) modulation technique combined with Quadrature Amplitude Modulation (QAM) modulation scheme to obtain maximum spectral efficiency (SE). In the receiving system, we utilize the sparse-structured reservoir computing post-equalization algorithm to achieve superior equalization performance on the basis of the traditional post-equalization algorithm. The experimental results indicate that this quasi-real-time communication system has achieved a signal transmission rate of 113.175Gbps. To the best of our knowledge, this work has set a record in the field of high-speed visible light laser communication. Therefore, the laser communication system constructed by this work, with its flexibility in deployment and high-speed performance, demonstrates the significant potential application of visible light laser communication in data center interconnection and high-speed indoor access networks.

Effects of cadmium exposure during pregnancy on genome-wide DNA methylation and the CREB/CREM pathway in the testes of male offspring rats.

This experimental study explored the multigenerational and transgenerational effects of cadmium (Cd) exposure during pregnancy on the testicular tissue and spermatogenesis of male offspring rats. CdCl2 at different doses (0, 0.5, 1, 2 mg/kg/day) were dispensed to pregnant SD rats, thus producing generation F1. Adult females in F1 (PND 56) were mated with untreated fertile males so as to produce generation F2. Likewise, adult females in F2 were mated to produce generation F3. Damages to testicular tissue were observed in all the three generations, with serum testosterone (T) increased in F2 and F3. Notably, the genome-wide DNA methylation level in the testicular tissue of F1 was altered, as was the expression of F1-F3 methyltransferases. In addition, the expression of Creb/Crem pathway, a pathway critical for the metamorphosis from postmeiotic round spermatocytes to spermatozoa, was also remarkably altered in the three generations. In concludion, prenatal Cd exposure might bring multigenerational and transgenerational toxic effects to testes via genome-wide DNA methylation and the regulation of CREB/CREM pathway.

One-bit quantization delta-sigma modulation-based autoencoder for power-efficient free-space communication.

This Letter proposes a novel, to the best of our knowledge, approach utilizing a delta-sigma modulation (DSM)-based 1-bit autoencoder (AE) for efficient encoding and decoding in various channel conditions. Simulation analysis demonstrates the AE's ability to mitigate noise by reducing a peak-to-average power ratio (PAPR) and enhancing an in-band power of the signals, particularly under low signal-to-noise ratios (SNRs). The AE-DSM achieves theoretical transmission performance even at SNRs below 6 dB. In a 40-m free-space link experiment, the AE-DSM exhibits an 8.4-dB lower bit error rate (BER) compared to 64QAM-DSM, enabling a transmission rate of 1.31 Gbps. Furthermore, the 1-bit AE-DSM significantly reduces power consumption in the receiving analog-to-digital converter (ADC), facilitates transmission at low SNRs, and effectively mitigates nonlinear effects. Consequently, the DSM-based AE holds immense potential for future mobile fronthaul links.

Prenatal cadmium exposure has inter-generational adverse effects on Sertoli cells through the follicle-stimulating hormone receptor pathway.

In brief: Exposure to cadmium (Cd) during pregnancy can potentially harm the reproductive system of male offspring. This article shows that pregnant woman should be protected from cadmium exposure. Abstract: Exposure to cadmium (Cd) during pregnancy can potentially harm the reproductive system of male offspring, although the full extent of its heritable effects remains partially unresolved. In this study, we examined the inter-generational impacts of Cd using a distinct male-lineage generational model. Pregnant Sprague-Dawley female rats (F0) were administered control or cadmium chloride (0.5, 1 and 2 mg/day) via intra-gastric administration from gestation day 1 to 20. Subsequently, the first filial generation (F1) male rats were mated with untreated females (not exposed to Cd) to produce the second filial generation (F2). Histopathological analysis of the F1 and F2 generations revealed abnormal testicular development, while ultrastructural examination indicated damage to Sertoli cells. Cd exposure also led to alterations in serum hormone levels (gonadotropin-releasing hormone, follicle-stimulating hormone) and reduced follicle-stimulating hormone receptor (FSHR) protein expression in Sertoli cells in the F1 generation. Furthermore, Cd affected the mRNA and protein expression of FSHR pathway factors and DNA methyltransferase, albeit with distinct patterns and inconsistencies observed between the F1 and F2 generations. Overall, our findings indicate that prenatal Cd exposure, using a male-lineage transmission model, can induce inter-generational effects on male reproduction, particularly by causing toxicity in Sertoli cells. This effect appears to be primarily mediated through disruptions in the FSHR pathway and changes in DNA methyltransferase activity in the male testes.

11.2 Gbps 100-meter free-space visible light laser communication utilizing bidirectional reservoir computing equalizer.

In this paper, we introduce an innovative post-equalization technique leveraging bidirectional reservoir computing (BiRC), and apply it to waveform-to-symbol level equalization for visible light laser communication for the first time. This strategy is more resistant to nonlinearities compared to traditional equalizers like least mean square (LMS) equalizer, while requiring less training time and fewer parameters than neural network (NN) -based equalizers. Through this approach, we successfully conduct a 100-meter transmission of a 32-amplitude phase shift keying (32APSK) signal using a green laser operating at a wavelength of 520 nm. Remarkably, our system achieves a high data rate of 11.2 Gbps, all while maintaining a satisfying bit error rate (BER) below the 7% hard decision forward error correction (HD-FEC) threshold of 3.8E-3.

Activation of Gonadotropin-releasing Hormone Receptor Impedes the Immunosuppressive Activity of Decidual Regulatory T Cells via Deactivating the Mechanistic Target of Rapamycin Signaling.

Understanding maternal immune tolerance is crucial for the development of therapeutics for immunological pregnancy complications. Decidual regulatory T cells (Tregs) play a pivotal role in the maintenance of maternal immune tolerance. Using a murine allogeneic pregnancy model in the current study, we identified the up-regulation of gonadotropin-releasing hormone receptor (GnRHR) in decidual T cell subsets including CD4+ conventional T cells, CD8+ T cells, and CD4+Foxp3+ Tregs. Using a lentivirus-mediated GnRHR overexpression system and a GnRHR agonist, we found that GnRHR activation decreased the expression of Treg functional molecules such as IL10 (IL-10), IL-35 subunit EBI3 (Ebi3), IL2RA (CD25), TNFRSF18 (GITR), ICOS, and Treg master regulator FOXP3. The functional analysis indicated that GnRHR activation impairs the ability of Tregs to inhibit conventional T cell proliferation. We also revealed that GnRHR activation suppressed the mechanistic target of rapamycin (mTOR) signaling in GnRHR-overexpressing splenic Tregs (Wild type C57BL/6 J background) and decidual Tregs. MHY1485, a potent mTOR activator, effectively abolished the effect of the GnRHR agonist and promoted the immunosuppressive capability of Tregs. Furthermore, in an adoptive transfer model, Treg-specific GnRHR knockdown increased Foxp3 expression in decidual Tregs while decreasing the production of IFN-γ and IL-17 in decidual effector CD4+ T cells and reducing the production of IFN-γ in decidual effector CD8+ T cells. Taken together, the present study unveils a novel mechanism by which the immunosuppressive function of decidual Tregs is modulated, and deepens our understanding of maternal immune tolerance.

Icariin induces apoptosis in mouse MLTC-10 Leydig tumor cells through activation of the mitochondrial pathway and down-regulation of the expression of piwil4.

The Leydig cell tumor, derived from interstitial cells, is a rare neoplasm. In most cases, Leydig cell tumors are benign, however, if the tumor is malignant, no effective treatments are currently available. In this study, we aimed to evaluate the effects of icariin on the growth of the mouse Leydig tumor cell line MLTC-1 and to examine its underlying mechanism. Icariin caused a dose-dependent decrease in the viability of MLTC-1 cells, which coincided with an increase in cell apoptosis through regulation of the expression of Bcl-2/Bax and cytochrome c, activation of caspase-9 and -3. Moreover, the pro-apoptotic effect of icariin on MLTC-1 cells is related to piwil4, since icariin induced a decrease in piwil4 protein expression and piwil4 silencing significantly enhanced the cytotoxic effects of icariin in MLTC-1 cells. These findings suggest a novel anticancer effect of icariin in Leydig cell tumor through activation of the mitochondrial pathway and down-regulation of the expression of piwil4.

Expression of proliferin-related protein in testis and the biological significance in testosterone production.

Proliferin-related protein (PRP) was originally identified as an angiogenesis inhibitor in mouse placentas. Indeed, the tissue expression of PRP has mainly been documented in placentas. We report herein for the first time that PRP is expressed in male rat testes. Immunocytochemical and in situ hybridization results showed positive PRP immunostaining in Leydig cells. Immunofluorescent staining of PRP in the TM3 Leydig cell line indicates that PRP is located within the cytoplasm. The expression pattern of PRP in rat testis exhibited an age-related increase. HCG significantly up-regulated the level of expression of PRP in TM3 cells via the PKA pathway. To elucidate the function of PRP, experiments were conducted to examine the consequences of lentiviral-mediated RNA interference (RNAi) of PRP on testosterone production and expression of several genes involved in steroidogenesis. PRP silencing caused a decrease in HCG-stimulated testosterone production. In addition, PRP silencing attenuated the increase in PRLR mRNA following HCG stimulation. Moreover, the enhanced effect of PRL on HCG-induced testosterone production was also weakened following PRP silencing, indicating that PRP may be involved in PRL function through an effect on PRL receptor expression in response to stimuli. Taken together, these data suggest that PRP is regulated by HCG and plays roles in male reproduction, such as testosterone production.

A novel loss-of-function DDAH1 promoter polymorphism is associated with increased susceptibility to thrombosis stroke and coronary heart disease.

RATIONALE: Asymmetrical dimethylarginine (ADMA), an endogenous arginine analogue, inhibits nitric oxide synthases and plays an important role in endothelial dysfunction. OBJECTIVE: In the present study, we tested whether a novel genetic variant in dimethylarginine dimethylaminohydrolase 1 (DDAH1), an important ADMA hydrolyzing gene, was associated with stroke and coronary heart disease (CHD) susceptibility in the Chinese Han population. METHODS AND RESULTS: By resequencing, we identified a novel 4-nucleotide deletion/insertion variant in the DDAH1 promoter. The insertion allele disrupted binding of metal-regulatory transcription factor 1, which resulted in significant reduction of in vitro DDAH1 transcriptional activity and in vivo DDAH1 mRNA level, and in turn, increased plasma ADMA level and the ratio of ADMA to L-arginine. We initially genotyped the polymorphism in 1388 stroke patients and 1027 controls as well as 576 CHD patients and 557 controls and then replicated our study in additional independent case-control cohorts comprising 961 stroke patients and 822 controls and 482 CHD patients and 1072 controls. We identified that the -396 4N ins allele was significantly associated with increased risk of thrombosis stroke and CHD after adjusting for environmental factors in both samples for both diseases (thrombosis stroke discovery set: odds ratio [OR]=1.35, P=0.032; replication set: OR=1.51, P=0.006; CHD discovery set: OR=1.45, P=0.035; replication set: OR=1.47, P=0.003). CONCLUSIONS: Our results suggest that the DDAH1 loss-of-function polymorphism is associated with both increased risk of thrombosis stroke and CHD.