Physiological responses of Porphyra haitanesis to different copper and zinc concentrations

No presente estudo foram investigadas as respostas fisiológicas da alga vermelha Porphyra haitanesis às elevadas concentrações de cobre (acima de 50 μM) e de zinco (acima de 100 μM). Os resultados mostram que os efeitos de Cu2+ e Zn2+ sobre o crescimento, pigmentos fotossintéticos (clorofilas e carotenóides), ficobiliproteína e metabolismo (o espectro de emissão de fluorescência e as atividades do fotossistema) não seguem o mesmo padrão. A taxa de crescimento relativo foi inibida por diferentes concentrações de Cu2+ e, em presença de Zn2+, aumentou ligeiramente em baixas concentrações (abaixo de 10 μM) e foi inibida em altas concentrações. Por outro lado, os teores de ficoeritrina apresentaram leve aumento em concentrações relativamente baixas de Cu2+ e Zn2+ (até 1 μM Cu2+ e até 20 μM Zn2+, respectivamente) e foram inibidas por altas concentrações. Além disso, tanto a fotossíntese quanto a respiração mostraram aumento nas trocas de oxigênio em resposta às concentrações relativamente baixas de Cu2+ (até 1 μM) e de Zn2+ (até 10 μM), além da redução em concentrações relativamente altas desses metais. Adicionalmente, as atividades fotoredutoras e as emissões de fluorescência do fotossistema II (PSII) foram incrementadas em baixas concentrações de Cu2+ (até 0,1 μM) e de Zn2+ (até 10 μM) e inibidas por altas concentrações. Desta forma, a intensidade da fluorescência da clorofila-a e dos centros de reação ativa PSII seguiram um padrão semelhante em resposta às elevadas concentrações de Cu2+ e Zn2+. Esses resultados sugerem que baixas concentrações de Cu2+ e Zn2+ afetam o metabolismo de P. haitanesis, que se torna inibido por altas concentrações desses metais.In the present study, several physiological responses of the red marine alga Porphyra haitanesis to elevated concentrations of copper (up to 50 μM) and zinc (up to 100 μM) were investigated. Our results showed that the effects of Cu2+ and Zn2+ on growth, photosynthetic pigments (chlorophylls and carotenoids), phycobiliprotein and metabolism (the fluorescence emission spectra and the activities of photosystemII) did not follow the same pattern. The relative growth rate was inhibited by different concentrations of Cu2+, and was slightly increased at lower concentrations (up to 10 μM) and inhibited at higher Zn2+concentrations. On the other hand, the phycoerythrin contents were slightly increased at relatively low concentrations (up to 1 μM Cu2+ or 20 μM Zn2+) and inhibited by high Cu2+ and Zn2+ concentrations. Moreover, photosynthesis and respiration showed an increase in the amount of oxygen exchange in response to relatively low Cu2+ (up to 1 μM) and Zn2+ concentrations (up to 10 μM), and a reduction to relatively high Cu2+ and Zn2+ concentrations. Oxygen evolution was more sensitive than oxygen uptake to Cu2+ and Zn2+. In addition, the photoreductive activities and fluorescence emission of photosystem II (PS II) were enhanced by lower concentrations of Cu2+ (up to 0.1 μM) and Zn2+ (up to 10 μM) and inhibited by higher concentrations. Furthermore, the intensity of chlorophyll a fluorescence and the active PSII reaction centers followed a similar pattern in response to elevated concentrations of Cu2+ and Zn2+. These results suggest that lower concentrations of Cu2+ and Zn2+ affected the metabolism of P. haitanesis, which was inhibited by higher concentrations of these metals

Solving Multidimensional 0-1 Knapsack Problem with Time-Free Tissue P Systems

Tissue P system is a class of parallel and distributed model; a feature of traditional tissue P system is that the execution time of certain biological processes is very sensitive to environmental factors that might be hard to control. In this work, we construct a family of tissue P systems that works independently from the values associated with the execution times of the rules. Furthermore, we present a time-free efficient solution to multidimensional 0-1 knapsack problem by timed recognizer tissue P systems

Gut microbiota and therapy for obesity and type 2 diabetes

There has been a major increase in Type 2 diabetes and obesity in many countries, and this will lead to a global public health crisis, which not only impacts on the quality of life of individuals well but also places a substantial burden on healthcare systems and economies. Obesity is linked to not only to type 2 diabetes but also cardiovascular diseases, musculoskeletal disorders, and certain cancers, also resulting in increased medical costs and diminished quality of life. A number of studies have linked changes in gut in obesity development. Dysbiosis, a deleterious change in gut microbiota composition, leads to altered intestinal permeability, associated with obesity and Type 2 diabetes. Many factors affect the homeostasis of gut microbiota, including diet, genetics, circadian rhythms, medication, probiotics, and antibiotics. In addition, bariatric surgery induces changes in gut microbiota that contributes to the metabolic benefits observed post-surgery. Current obesity management strategies encompass dietary interventions, exercise, pharmacotherapy, and bariatric surgery, with emerging treatments including microbiota-altering approaches showing promising efficacy. While pharmacotherapy has demonstrated significant advancements in recent years, bariatric surgery remains one of the most effective treatments for sustainable weight loss. However, access to this is generally limited to those living with severe obesity. This underscores the need for non-surgical interventions, particularly for adolescents and mildly obese patients. In this comprehensive review, we assess longitudinal alterations in gut microbiota composition and functionality resulting from the two currently most effective anti-obesity treatments: pharmacotherapy and bariatric surgery. Additionally, we highlight the functions of gut microbiota, focusing on specific bacteria, their metabolites, and strategies for modulating gut microbiota to prevent and treat obesity. This review aims to provide insights into the evolving landscape of obesity management and the potential of microbiota-based approaches in addressing this pressing global health challenge

Electro-Acupuncture Affects the Activity of the Hypothalamic-Pituitary-Ovary Axis in Female Rats

Hypothalamic-pituitary-ovary (HPO) axis is a dominant system controlling ovulation during puberty. Electro-acupuncture (EA) has been widely used to cure the reproductive diseases associated with endocrinological disorders. However, whether EA treatment affects HPO axis activity of physiological animals and induces alterations on the hormones in the HPO axis was also unclear. Here, we performed the EA stimuli on bilateral acupoints of Sanyinjiao (SP6) and Zusanli (ST36) on female virgin rats every 3 days and for a total of 5 times. The results showed that GnRH levels in hypothalamus were greatly upregulated in EA-treated rats than untreated animals at day 7 and 13. The serum levels for FSH and LH were severely reduced after EA treatment compared with EA-untreated animals at day 1, while they were greatly increased at day 7 and 13. The serum concentrations of 17β-estradiol were lower in EA-treated rats versus untreated animals at day 7, while they were higher in EA-treated rats than other groups at day 13. However, the progesterone concentrations were lower in EA-treated rats than Control and Sham-EA rats both at day 7 and 13. More importantly, we found that the prostaglandin E2 level in serum was reduced in EA-treated rats versus untreated rats at day 1, while they were upregulated at day 7 and 13. Conversely, the norepinephrine level in serum was increased at day 1, while they were decreased greatly in EA-treated rats versus untreated rats at day 7 and 13. The current results demonstrated that EA could modulate homeostasis of HPO axis in physiologic rats, which would be useful to clarify the mechanisms of EA application on pathological and physiological animals or human

An integrated transcriptomic and computational analysis for biomarker identification in gastric cancer

This report describes an integrated study on identification of potential markers for gastric cancer in patients’ cancer tissues and sera based on: (i) genome-scale transcriptomic analyses of 80 paired gastric cancer/reference tissues and (ii) computational prediction of blood-secretory proteins supported by experimental validation. Our findings show that: (i) 715 and 150 genes exhibit significantly differential expressions in all cancers and early-stage cancers versus reference tissues, respectively; and a substantial percentage of the alteration is found to be influenced by age and/or by gender; (ii) 21 co-expressed gene clusters have been identified, some of which are specific to certain subtypes or stages of the cancer; (iii) the top-ranked gene signatures give better than 94% classification accuracy between cancer and the reference tissues, some of which are gender-specific; and (iv) 136 of the differentially expressed genes were predicted to have their proteins secreted into blood, 81 of which were detected experimentally in the sera of 13 validation samples and 29 found to have differential abundances in the sera of cancer patients versus controls. Overall, the novel information obtained in this study has led to identification of promising diagnostic markers for gastric cancer and can benefit further analyses of the key (early) abnormalities during its development

Epithelial endoplasmic reticulum stress orchestrates a protective IgA response.

Immunoglobulin A (IgA) is the major secretory immunoglobulin isotype found at mucosal surfaces, where it regulates microbial commensalism and excludes luminal factors from contacting intestinal epithelial cells (IECs). IgA is induced by both T cell-dependent and -independent (TI) pathways. However, little is known about TI regulation. We report that IEC endoplasmic reticulum (ER) stress induces a polyreactive IgA response, which is protective against enteric inflammation. IEC ER stress causes TI and microbiota-independent expansion and activation of peritoneal B1b cells, which culminates in increased lamina propria and luminal IgA. Increased numbers of IgA-producing plasma cells were observed in healthy humans with defective autophagy, who are known to exhibit IEC ER stress. Upon ER stress, IECs communicate signals to the peritoneum that induce a barrier-protective TI IgA response.Wellcome Trust Senior Investigator Award 106260/Z/14/Z HORIZON2020/European Research Council Consolidator Grant 64888