A Triple-Mode Flexible E-Skin Sensor Interface for Multi-Purpose Wearable Applications

This study presents a flexible wireless electronic skin (e-skin) sensor system that includes a multi-functional sensor device, a triple-mode reconfigurable readout integrated circuit (ROIC), and a mobile monitoring interface. The e-skin device's multi-functionality is achieved by an interlocked micro-dome array structure that uses a polyvinylidene fluoride and reduced graphene oxide (PVDF/RGO) composite material that is inspired by the structure and functions of the human fingertip. For multi-functional implementation, the proposed triple-mode ROIC is reconfigured to support piezoelectric, piezoresistance, and pyroelectric interfaces through single-type e-skin sensor devices. A flexible system prototype was developed and experimentally verified to provide various wireless wearable sensing functions-including pulse wave, voice, chewing/swallowing, breathing, knee movements, and temperature-while their real-time sensed data are displayed on a smartphone

SGLT2 is not expressed in pancreatic α- and β-cells, and its inhibition does not directly affect glucagon and insulin secretion in rodents and humans.

OBJECTIVE: Sodium-glucose cotransporter 2 (SGLT2) inhibitors (SGLT2i), or gliflozins, are anti-diabetic drugs that lower glycemia by promoting glucosuria, but they also stimulate endogenous glucose and ketone body production. The likely causes of these metabolic responses are increased blood glucagon levels, and decreased blood insulin levels, but the mechanisms involved are hotly debated. This study verified whether or not SGLT2i affect glucagon and insulin secretion by a direct action on islet cells in three species, using multiple approaches. METHODS: We tested the in vivo effects of two selective SGLT2i (dapagliflozin, empagliflozin) and a SGLT1/2i (sotagliflozin) on various biological parameters (glucosuria, glycemia, glucagonemia, insulinemia) in mice. mRNA expression of SGLT2 and other glucose transporters was assessed in rat, mouse, and human FACS-purified α- and β-cells, and by analysis of two human islet cell transcriptomic datasets. Immunodetection of SGLT2 in pancreatic tissues was performed with a validated antibody. The effects of dapagliflozin, empagliflozin, and sotagliflozin on glucagon and insulin secretion were assessed using isolated rat, mouse and human islets and the in situ perfused mouse pancreas. Finally, we tested the long-term effect of SGLT2i on glucagon gene expression. RESULTS: SGLT2 inhibition in mice increased the plasma glucagon/insulin ratio in the fasted state, an effect correlated with a decline in glycemia. Gene expression analyses and immunodetections showed no SGLT2 mRNA or protein expression in rodent and human islet cells, but moderate SGLT1 mRNA expression in human α-cells. However, functional experiments on rat, mouse, and human (29 donors) islets and the in situ perfused mouse pancreas did not identify any direct effect of dapagliflozin, empagliflozin or sotagliflozin on glucagon and insulin secretion. SGLT2i did not affect glucagon gene expression in rat and human islets. CONCLUSIONS: The data indicate that the SGLT2i-induced increase of the plasma glucagon/insulin ratio in vivo does not result from a direct action of the gliflozins on islet cells

The lack of functional nicotinamide nucleotide transhydrogenase only moderately contributes to the impairment of glucose tolerance and glucose-stimulated insulin secretion in C57BL/6J vs C57BL/6N mice.

Aims/hypothesis: Nicotinamide nucleotide transhydrogenase (NNT) is involved in mitochondrial NADPH production and its spontaneous inactivating mutation (NntTr [Tr, truncated]) is usually considered to be the main cause of the lower glucose tolerance of C57BL/6J vs C57BL/6N mice. However, the impact of this mutation on glucose tolerance remains disputed. Here, we singled out the impact of NntTr from that of other genetic variants between C57BL/6J and C57BL/6N mice on mitochondrial glutathione redox state (EGSH), glucose-stimulated insulin secretion (GSIS) and glucose tolerance. Methods: Male and female N5BL/6J mice that express wild-type Nnt (NntWT) or NntTr (N5-WT and N5-Tr mice) on the C57BL/6J genetic background were obtained by crossing N5BL/6J NntWT/Tr heterozygous mice. C57BL/6J and C57BL/6N mice were from Janvier Labs. The Nnt genotype was confirmed by PCR and the genetic background by whole genome sequencing of one mouse of each type. Glucose tolerance was assessed by IPGTT, ITT and fasting/refeeding tests. Stimulus-secretion coupling events and GSIS were measured in isolated pancreatic islets. Cytosolic and mitochondrial EGSH were measured using the fluorescent redox probe GRX1-roGFP2 (glutaredoxin 1 fused to redox-sensitive enhanced GFP). Results: The Nnt genotype and genetic background of each type of mouse were confirmed. As reported previously in C57BL/6N vs C57BL/6J islets, the glucose regulation of mitochondrial (but not cytosolic) EGSH and of NAD(P)H autofluorescence was markedly improved in N5-WT vs N5-Tr islets, confirming the role of NNT in mitochondrial redox regulation. However, ex vivo GSIS was only 1.2-1.4-times higher in N5-WT vs N5-Tr islets, while it was 2.4-times larger in C57BL/6N vs N5-WT islets, questioning the role of NNT in GSIS. In vivo, the ITT results did not differ between N5-WT and N5-Tr or C57BL/6N mice. However, the glucose excursion during an IPGTT was only 15-20% lower in female N5-WT mice than in N5-Tr and C57BL/6J mice and remained 3.5-times larger than in female C57BL/6N mice. Similar observations were made during a fasting/refeeding test. A slightly larger (~30%) impact of NNT on glucose tolerance was found in males. Conclusions/interpretation: Although our results confirm the importance of NNT in the regulation of mitochondrial redox state by glucose, they markedly downsize the role of NNT in the alteration of GSIS and glucose tolerance in C57BL/6J vs C57BL/6N mice. Therefore, documenting an NntWT genotype in C57BL/6 mice does not provide proof that their glucose tolerance is as good as in C57BL/6N mice

Sensor Interface for Electromyogram with Wavelet Filter

This paper presents electromyogram(EMG) sensing interface with wavelet process. Wavelet process is effective to analyze EMG signal because it provides signal information in frequency domain. The power of EMG signal is concentrated in 50~150Hz range. By using wavelet transform filters, the EMG signal is decomposed in several ranges of frequency. In this process, immunity to motion artifacts is enhanced and analyzing an EMG with various frequency ranges gives more information about specific movement. the amount of data is decreased because down sampling is used in wavelet transform process. Thus, it improves communication efficiency. The proposed interface is designed in 0.18??m CMOS process

Acupuncture treatment for functional gastrointestinal disorders: Identification of major acupoints using network analysis

Background: Using network analysis, we sought to determine the acupoints most commonly used to treat functional gastrointestinal disorders (FGIDs), particularly functional dyspepsia (FD) and irritable bowel syndrome (IBS). Methods: To explore the acupoint patterns used for FGID, data on acupoint combinations for FD and IBS were gathered from systematic reviews. Network analysis was used to determine the degree, closeness centrality, betweenness centrality, and eigenvector centrality of each acupoint. The most common acupoint combinations for FD and IBS were examined based on the eigenvector centrality. Results: Network analysis revealed that CV12, ST25, ST36, CV10, and LR3, which had the highest eigenvector centrality values, were the main acupoints for treating FGID. CV12 was the main acupoint for treating FD, while ST25 was the hub acupoint for treating IBS in the abdomen. ST36, LR3, and PC6 were the key peripheral acupoints for FD and IBS. Conclusions: Using network analysis, we provided data that will aid the selection of both general and specific acupoints for FD and IBS, along with spatial information (i.e., the positions of acupoints on a body map). These findings could be applied in future acupuncture research on therapy for gastrointestinal system dysfunction. They may also help bridge the gap between the traditional meridian theory, which assumes that there is a link between diseases/symptoms and the specific body region being treated, and real-world clinical evidence

Looking into the labyrinth of gender inequality: women physicians in academic medicine

Context Gender inequality remains prevalent worldwide in academic medicine. A closer look into women physicians’ gendered experiences through the lens of culture is necessary to advance understanding of gender inequality in this context. Relatively few studies, however, have investigated how social and cultural practices implicitly yet significantly affect gender inequality throughout women physicians’ careers. Objectives This study aimed to investigate the lived experiences of South Korean women physicians working in academic medicine and to focus on social and cultural influences on the gendered process of their career journeys. The study will extend our understanding of gender inequality in academic medicine through an in‐depth analysis of social and cultural practices that affect the phenomenon. Methods We conducted a qualitative study utilising a grounded theory approach. Twenty‐one women physicians participated in semi‐structured interviews. Data were recorded, transcribed and analysed through a process of constant comparison using grounded theory to extract themes. Results Junior women physicians were more vulnerable to gender discrimination and channelled to ‘ghettos’ through the seniority‐based, patriarchal, collectivist and business hospital culture in South Korea. Under pressure to excel at work, they had no work–family balance and experienced identity crises as competent doctors and mothers. They felt themselves to be ‘othered’ in multiple cultural contexts, including school ties, rankism and a culture of after‐work gatherings. Minimal levels of leadership aspiration created a vicious cycle of a lack of social networking and mentoring. Pursuing individual excellence, they attributed their struggles to personal choices and rarely sought organisational support. Conclusions The dynamics of cultural and social practices constantly and implicitly recreate mechanisms to maintain gender inequality in academic medicine in South Korea. Planned culture changes at individual, organisational and national levels are imperative to discontinue the vicious cycle that exists in the labyrinth of women physicians’ career development in academic medicine