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Abstract Background The cycle threshold (Ct) value is inversely proportional to the number of copies of the target region in a sample, suggesting that a low Ct value indicates a high pathogen load. The relationship between Ct value and clinical presentation in children with pertussis is not well-defined. Methods We investigated the relationships between the Ct value of nasopharyngeal samples positive for Bordetella pertussis deoxyribonucleic acid via real-time polymerase chain reaction (PCR), collected from children on admission and their adult family members between May 2022 and March 2024 at Hangzhou Children’s Hospital, China. The study focused on the correlation between Ct value and clinical presentation in children with pertussis. Results The Ct value was positively correlated with age (r = 0.362, P = 0.001). The mean Ct value for children with pertussis was 28.0 (range: 22.0–32.0), which was lower than the 32.0 (range: 30.0–34.0) observed in adults. Ct value was inversely correlated with length of stay, an indicator of disease severity (r = -0.356, P = 0.001). Logistic regression analyses revealed that both Ct value (OR: 0.891, 95% CI: 0.799–0.993, P = 0.036) and white blood cell count (OR: 1.127, 95% CI: 1.005–1.263, P = 0.040) were independently associated with severity of pertussis. Conclusions Real-time PCR Ct values at initial diagnosis for pertussis may potentially predict severe disease outcomes in children.

Abstract NRAS mutations are most frequently observed in hematological malignancies and are also common in some solid tumors such as melanoma and colon cancer. Despite its pivotal role in oncogenesis, no effective therapies targeting NRAS has been developed. Targeting NRAS localization to the plasma membrane (PM) is a promising strategy for cancer therapy, as its signaling requires PM localization. However, the process governing NRAS translocation from the Golgi apparatus to the PM after lipid modification remains elusive. This study identifies GOLGA7 as a crucial factor controlling NRAS’ PM translocation, demonstrating that its depletion blocks NRAS, but not HRAS, KRAS4A and KRAS4B, translocating to PM. GOLGA7 is known to stabilize the palmitoyltransferase ZDHHC9 for NRAS and HRAS palmitoylation, but we found that GOLGA7 depletion does not affect NRAS’ palmitoylation level. Further studies show that loss of GOLGA7 disrupts NRAS anterograde trafficking, leading to its cis-Golgi accumulation. Remarkably, depleting GOLGA7 effectively inhibits cell proliferation in multiple NRAS-mutant cancer cell lines and attenuates NRASG12D-induced oncogenic transformation in vivo. These findings elucidate a specific intracellular trafficking route for NRAS under GOLGA7 regulation, highlighting GOLGA7 as a promising therapeutic target for NRAS-driven cancers.

Abstract The two key problems of the in‐band ripples and out‐of‐band suppression are proposed in the design of the SAW yarn tension sensor and the methods of decreasing them are achieved. The unbalanced split‐electrode interdigital transducers (IDT) are designed so that the total phase of the regenerated reflection wave and mass load feedback is close to 180°, leading to an effective reduction of the in‐band ripples effect characterised by the sensor frequency response. The engraved bi‐directional slots on the back of the substrate can block the propagation path of the bulk acoustic wave (BAW) to a certain extent, reducing the influence of BAW propagation and suppressing the out‐of‐band suppression of the frequency response. The experimental results show that the SAW yarn tension sensor with the unbalanced split‐electrode IDT can reduce the in‐band ripples from 23.34 to 0.93 dB, and the engraved bi‐directional slots can suppress the out‐of‐band suppression from 28.03 to 7.71 dB.

Magnetic tunnel junction (MTJ) sensors have been one of the excellent candidates for magnetic field detection due to their high sensitivity and compact size. In this paper, we design a magnetometer with in situ magnetic feedback consisting of an MTJ sensor. To analyze and evaluate the detectivity of the MTJ magnetometer, a noise model of the MTJ sensor in the magnetometer without magnetic feedback is first developed. Then, the noise model of the MTJ magnetometer with in situ magnetic feedback is also established, including the noises of the MTJ sensor and the signal conditioning circuit, as well as the feedback circuit. The equivalent noise model of the MTJ magnetometer with in situ magnetic feedback is evaluated through nonlinear fitting for the noise voltage spectrum. Although the noise generated by the MTJ sensor is much greater than that of the signal conditioning circuit, the noise introduced by the feedback coils into the MTJ sensor is slightly more than twice that generated by the MTJ sensor itself. The measurement results show that the detectivity of the MTJ magnetometer with in situ magnetic feedback reaches 526 pT/Hz1/2 at 10 Hz. The equivalent noise analysis method presented in this paper is suitable for the detectivity analysis of magnetometers with magnetic feedback.

TP53-induced glycolysis and apoptosis regulator (TIGAR) alleviates oxidative stress and protects against ischemic neuronal injury by shifting glucose metabolism into the pentose phosphate pathway (PPP). However, the brain alters glucose metabolism from PPP to glycolysis during prolonged ischemia. It is still unknown whether and how TIGAR exerts the antioxidant activity and neuroprotection in prolonged ischemic brains. Here, we determined the significant upregulation of TIGAR that was proportional to the duration of ischemia. However, TIGAR failed to upregulate the NADPH level but still alleviated oxidative stress in neuronal cells with prolonged oxygen glucose-deprivation (OGD). Furthermore, inhibiting PPP activity, either by the expression of mutant TIGAR (which lacks enzymatic activity) or by silencing Glucose 6-phosphate dehydrogenase, still retained antioxidant effects and neuroprotection of TIGAR with prolonged OGD. Intriguingly, TIGAR-induced autophagy alleviated oxidative stress, contributing to neuron survival. Further experiments indicated that TIGAR-induced autophagy neutralized oxidative stress by activating Nrf2, which was cancelled by ML385 or Nrf2 knockdown. Remarkably, either Atg7 deletion or Nrf2 silencing abolished the neuroprotection of TIGAR in mice with prolonged ischemia. Taken together, we found a PPP-independent pathway in which TIGAR alleviates oxidative stress. TIGAR induces autophagy and, thus, activates Nrf2, offering sustainable antioxidant defense in brains with extended ischemia. This previously unexplored mechanism of TIGAR may serve as a critical compensation for antioxidant activity caused by the lack of glucose in ischemic stroke.

Neurotoxins generally inhibit or promote the release of neurotransmitters or bind to receptors that are located in the pre- or post-synaptic membranes, thereby affecting physiological functions of synapses and affecting biological processes. With more and more research on the toxins of various origins, many neurotoxins are now widely used in clinical treatment and have demonstrated good therapeutic outcomes. This review summarizes the structural properties and potential pharmacological effects of neurotoxins acting on different components of the synapse, as well as their important clinical applications, thus could be a useful reference for researchers and clinicians in the study of neurotoxins.