Flexible pressure sensors have aroused tremendous attention, owing to their broad applications in healthcare, robotics, and prosthetics. So far, it remains a critical challenge to develop low-cost and controllable microstructures for flexible pressure sensors. Herein, a high-sensitivity and low-cost flexible piezoresistive sensor was developed by combining a controllable graphene-nanowalls (GNWs) wrinkle and a polydimethylsiloxane (PDMS) elastomer. For the GNWs–PDMS bilayer, the vertically grown GNWs film can effectively improve the interface strength and form delamination-free conformal wrinkles. More importantly, a controllable microstructure can be easily tuned through the thermal wrinkling method. The wrinkled graphene-nanowalls (WG) piezoresistive sensor has a high sensitivity (S = 59.0 kPa–1 for the 0–2 kPa region and S = 4.8 kPa–1 for the 2–20 kPa region), a fast response speed (<6.9 ms), and a low limit of detection (LOD) of 2 mg (∼0.2 Pa). The finite element method was used to analyze the working mechanism of the sensor, which revealed that the periods of the wrinkles play a dominant role in the performances of the sensors. These prominent merits enable wrinkled graphene sensors to successfully detect various signals from a weak stimulus to large pressures, for example, the detection of weak gas and plantar pressure. Furthermore, object manipulation, tactile imaging, and braille recognition applications have been demonstrated, showing their great potential in prosthetics limbs and intelligent robotics.

PURPOSE: This study investigated the association between background parenchymal enhancement (BPE) and pathologic response to neoadjuvant chemotherapy (NAC). METHODS: A total of 46 patients diagnosed with invasive breast cancer were analyzed. Each patient had three magnetic resonance imaging (MRI) studies, one pre-treatment and two follow-up (F/U) MRI studies. BPE was measured as the averaged enhancement of the whole fibroglandular tissues. The pre-treatment BPE and the changes in the F/U MRI were compared between patients achieving pathologic complete response (pCR) versus those not. Subgroup analyses based on age, estrogen receptor (ER), and human epidermal growth factor receptor 2 (HER2) status of their cancers were also performed. RESULTS: The pre-treatment BPE was higher in the pCR group than that in the non-pCR group. Compared to baseline, BPE at F/U-1 was significantly decreased in the pCR group but not in the non-pCR group. In subgroup analysis based on age, these results were seen only in the younger group (< 55 years old), not in the older group (≥ 55 years old). Older patients had a significantly lower pre-treatment BPE than younger patients. In analysis based on molecular biomarkers, a significantly decreased BPE at F/U-1 was only found in the ER-negative pCR group but not in the non-pCR, nor in the ER-positive groups. CONCLUSIONS: A higher pre-treatment BPE showing a significant decrease early after starting NAC was related to pCR in pre/peri-menopausal patients.

We previously showed that mitochondrial dysfunction (MtD) is involved in an aldosterone (Aldo)-induced podocyte injury. Here, the potential role of MtD in the initiation of podocyte damage was investigated. We detected the dynamic changes of urinary protein, urinary F2-isoprostane and renal malondialdehyde levels, kidney ultrastructure morphology, mitochondrial DNA (mtDNA) copy number, mitochondrial membrane potential (ΔΨm), and nephrin and podocin expressions in Aldo-infused mice. Aldo infusion first induced renal oxidative stress, as evidenced by increased levels of urinary F2-isoprostane and renal malondialdehyde, and MtD, as demonstrated by reduced mtDNA, ΔΨm, and ATP production. Later, at 5 days after Aldo infusion, proteinuria and podocyte injury began to appear. In cultured podocytes, Aldo or hydrogen peroxide (H2O2) induced MtD after 2-8 h of treatment, whereas the podocyte damage, as shown by decreased nephrin and podocin expressions, occurred later after 12 h of treatment. Thus Aldo treatment both in vitro and in vivo indicated that MtD occurred before podocyte damage. Additionally, MtDNA depletion by ethidium bromide or mitochondrial transcription factor A (TFAM) RNAi induced MtD, further promoting podocyte damage. TFAM expression was found to be reduced in Aldo-infused mice and Aldo-treated podocytes. Adenoviral vector-mediated overexpression of TFAM prevented Aldo-induced MtD and protected against podocyte injury. Together, these findings support MtD as an early event in podocyte injury, and manipulation of TFAM may be a novel strategy for treatment of glomerular diseases such as podocytopathy.

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