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1.
Entropy (Basel) ; 24(10)2022 Sep 22.
Artigo em Inglês | MEDLINE | ID: mdl-37420352

RESUMO

In order to further improve the information effectiveness of digital image transmission, an image-encryption algorithm based on 2D-Logistic-adjusted-Sine map (2D-LASM) and Discrete Wavelet Transform (DWT) is proposed. First, a dynamic key with plaintext correlation is generated using Message-Digest Algorithm 5 (MD5), and 2D-LASM chaos is generated based on the key to obtain a chaotic pseudo-random sequence. Secondly, we perform DWT on the plaintext image to map the image from the time domain to the frequency domain and decompose the low-frequency (LF) coefficient and high-frequency (HF) coefficient. Then, the chaotic sequence is used to encrypt the LF coefficient with the structure of "confusion-permutation". We perform the permutation operation on HF coefficient, and we reconstruct the image of the processed LF coefficient and HF coefficient to obtain the frequency-domain ciphertext image. Finally, the ciphertext is dynamically diffused using the chaotic sequence to obtain the final ciphertext. Theoretical analysis and simulation experiments show that the algorithm has a large key space and can effectively resist various attacks. Compared with the spatial-domain algorithms, this algorithm has great advantages in terms of computational complexity, security performance, and encryption efficiency. At the same time, it provides better concealment of the encrypted image while ensuring the encryption efficiency compared to existing frequency-domain methods. The successful implementation on the embedded device in the optical network environment verifies the experimental feasibility of this algorithm in the new network application.

2.
BMC Endocr Disord ; 21(1): 121, 2021 Jun 15.
Artigo em Inglês | MEDLINE | ID: mdl-34130678

RESUMO

BACKGROUND: Previous studies have indicated that women with a history of menstrual disorders have an increased risk of metabolic and cardiovascular diseases. This has been attributed to the high proportion of polycystic ovary syndrome (PCOS) among this group. The favorable effects of hormone replacement therapy (HRT) on serum lipid profiles and glucose homeostasis in postmenopausal women is widely accepted. Whether HRT can also show positive effects on metabolic homeostasis in menopausal women with prior menstrual disorders (a putative PCOS phenotype) has not been reported yet. The aim of the study was to compare the effects of HRT on glucose and lipid metabolism in peri- and postmenopausal women with prior menstrual disorders and controls who did not have prior menstrual disorders. METHODS: A retrospective multicenter study was conducted including 595 peri- and postmenopausal women who received HRT at four hospitals in the Zhejiang Province from May 31, 2010 to March 8, 2021. Participants were divided into the Normal menstruation group and the Menstrual disorders group according to their prior usual menstrual cycle pattern. Glucose and lipid metabolism indicators were assessed at baseline and after HRT. The results were compared between and within the groups, and data from peri- and postmenopausal women were analyzed separately. RESULTS: HRT significantly decreased fasting insulin and homeostasis model assessment of insulin resistance in perimenopausal users, and fasting plasma glucose levels in postmenopausal users with prior menstrual disorders, compared with baseline. Furthermore, HRT decreased low-density lipoprotein cholesterol, total cholesterol, fasting insulin, fasting plasma glucose and homeostasis model assessment of insulin resistance in both peri- and postmenopausal controls, compared with baseline. Nevertheless, no significant differences were observed in any of the glucose or lipid metabolism indicators at baseline and follow-up, as well as changes from baseline levels between menopausal women with and without prior menstrual disorders. CONCLUSIONS: HRT shows more obvious within-group improvements in glucose and lipid metabolism in controls, but there is no significant between-group difference. Further prospective studies are required for confirmation.


Assuntos
Biomarcadores/metabolismo , Glucose/metabolismo , Terapia de Reposição Hormonal/métodos , Metabolismo dos Lipídeos , Distúrbios Menstruais/tratamento farmacológico , Pós-Menopausa/metabolismo , Estudos de Casos e Controles , Feminino , Seguimentos , Humanos , Distúrbios Menstruais/metabolismo , Distúrbios Menstruais/patologia , Pessoa de Meia-Idade , Prognóstico , Estudos Retrospectivos
3.
Front Biosci (Landmark Ed) ; 25(11): 1974-1984, 2020 06 01.
Artigo em Inglês | MEDLINE | ID: mdl-32472767

RESUMO

Loss of pancreatic beta-cells by apoptosis appears to play an important role in the development of insulin deficiency and the onset and/or progression of the diabetes mellitus. To this end, we report that curcumin prevents high glucose (HG) induced oxidative stress and apoptosis in mouse pancreatic beta cells. Moreover, curcumin prevents HG induced increase in expression of CHOP, decrease in PCG-1a and phosphorylation of ERK1/2 (pERK1/2) without any effect on the phosphorylation levels of p38 and JNK. Moreover, similar to curcumin, blockade of pERK1/2 reduced the HG induced apoptosis in pancreatic beta cells. Overexpression of CHOP or siRNA knockdown of PCG-1a counteracted the effect of curcumin on HG induced apoptosis and oxidative stress. These results suggest that curcumin acts through CHOP/PCG-1a and ERK1/2 signaling to block the HG induced oxidative stress and apoptosis.


Assuntos
Apoptose/efeitos dos fármacos , Curcumina/farmacologia , MAP Quinases Reguladas por Sinal Extracelular/metabolismo , Glucose/farmacologia , Células Secretoras de Insulina/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/metabolismo , Fator de Transcrição CHOP/metabolismo , Animais , Anti-Inflamatórios não Esteroides/farmacologia , Linhagem Celular Tumoral , Curcumina/metabolismo , Glucose/metabolismo , Humanos , Células Secretoras de Insulina/metabolismo , Camundongos , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Coativador 1-alfa do Receptor gama Ativado por Proliferador de Peroxissomo/genética , Fosforilação/efeitos dos fármacos , Interferência de RNA , Fator de Transcrição CHOP/genética
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