Salt Restriction and Angiotensin-Converting Enzyme Inhibitor Improve the Responsiveness of the Small Artery in Salt-Sensitive Hypertension.

For salt-sensitive hypertension (SSH), salt restriction and angiotensin-converting enzyme (ACE) inhibitors are essential treatments, but their effect on the function of resistance arteries is unclear. Here, we present an intravital study to detect the effect of salt restriction and ACE inhibitors on the function of the mesenteric small artery (MSA) in SSH. Dahl salt-sensitive rats were randomized into the following groups: ACE inhibitor gavage, salt restriction, ACE inhibitor combined with salt restriction, and high-salt diet. After a 12-week intervention, the mesenteric vessels maintained their perfusion in vivo, and the changes in the diameter and blood perfusion of the MSAs to norepinephrine (NE) and acetylcholine (ACh) were detected. Switching from a high-salt diet to a low-salt diet (i.e., salt restriction) attenuated the vasoconstriction of the MSAs to NE and promoted the vasodilatation to ACh, while ACE inhibitor improved the vasodilatation more obviously. Pathologically, changes in local ACE, AT1R, and eNOS expression were involved in these processes induced by a high-salt diet. Our study suggests that salt restriction and ACE inhibitor treatment improve high salt intake-induced MSA dysfunction in SSH, and salt restriction is a feasible and effective treatment. Our findings may provide a scientific basis for the treatment of hypertension.

Management Strategy for Gallbladder Polypoid Lesions: Results of a 5-Year Single-Center Cohort Study.

INTRODUCTION: Controversy remains about the classification, differential diagnosis, and treatment strategy for gallbladder polypoid lesions (GPLs). This study sought to explore the individualized treatment strategy for GPLs. METHODS: We retrospectively studied 642 consecutive patients with GPLs from January 2015 to May 2020. Univariate and multivariable analyses were performed to explore the potential risk factors for neoplastic polyps. The outcome of laparoscopic gallbladder-preserving polypectomy (GPP) was evaluated and compared with that of laparoscopic cholecystectomy (LC). RESULTS: Of 642 enrolled patients, 572 underwent LC, and 70 underwent GPP. Pathologically, the majority of GPLs were cholesterol polyps (68.4%), followed by adenomyomatosis (19.9%), benign adenoma (7.3%), adenocarcinoma (3.6%), and rare pathological types (0.8%). Additionally, 66.3% (379/572) of the LC cases were classified as non-neoplastic, and 33.7% (193/572) neoplastic polyps. Multivariate analysis demonstrated that single polyps (OR 1.956, 95% CI: 1.121-3.412; p = 0.018), polyps located at the gallbladder fundus (OR 4.326, 95% CI: 2.179-8.591; p < 0.001), polyps not less than 14 mm (OR 2.833, 95% CI: 1.614-4.973; p < 0.001), and polyps with a broad base (OR 4.173, 95% CI: 1.743-9.990; p = 0.001) were independent risk factors for neoplastic polyps. The 5-year prospective results after GPP showed that the 1-year and 3-year polyp recurrence rates were 13.2% and 23.4%, respectively. CONCLUSION: The majority of GPLs are cholesterol or other benign lesions without malignant potential. LC is the main treatment procedure for GPLs with a high neoplastic risk. GPP is potentially feasible and could be an alternative management strategy for a group of GPLs patients who meet the selection criteria.

A pH-regulated fluorescence covalent organic framework for quantitative water content detection in methanol.

In this paper, we designed and synthesized a two-dimensional fluorescent covalent organic framework (TAPB-DMTP-COF) for the precise determination of H2O content in methanol. The COF was synthesized using two typical monomers by grinding method, which significantly reduced the synthesis time. By adjusting the pH value of the COF suspension to 4.0, the portion of the COF material structure is disrupted, thereby mitigating π-π stacking and resolving the aggregation-caused quenching (ACQ) effect. Consequently, the non-fluorescent TAPB-DMTP-COF exhibited blue-purple fluorescence emission in methanol. At the same time, it is observed that in the presence of H2O, there is a red shift in the maximum fluorescence emission peak of TAPB-DMTP-COF, which correlates with the H2O content within a specific range. Notably, this redshift demonstrates a linear relationship with H2O content from 4% to 80% in methanol. Our work presents novel insights for efficient analysis and detection of H2O content in methanol and could be used for H2O detection in other organic solvents.

Neuroprotective effect of astragalin via activating PI3K/Akt-mTOR-mediated autophagy on APP/PS1 mice.

As a small molecule flavonoid, astragalin (AST) has anti-inflammatory, anti-cancer, and anti-oxidation effects. However, the impact and molecular mechanism of AST in Alzheimer's disease (AD) are still not clear. This study aims to investigate the neuroprotective effect and mechanism of AST on APP/PS1 mice and Aß25-35-injured HT22 cells. In this study, we found that AST ameliorated cognitive dysfunction, reduced hippocampal neuronal damage and loss, and Aß pathology in APP/PS1 mice. Subsequently, AST activated autophagy and up-regulated the levels of autophagic flux-related protein in APP/PS1 mice and Aß25-35-induced injury in HT22 cells. Interestingly, AST down-regulated the phosphorylation level of PI3K/Akt-mTOR pathway-related proteins, which was reversed by autophagy inhibitors 3-Methyladenine (3-MA) or Bafilomycin A1 (Baf A1). At the same time, consistent with the impacts of Akt inhibitor MK2206 and mTOR inhibitor rapamycin, inhibited levels of autophagy in Aß25-35-injured HT22 cells were activated by the administration of AST. Taken together, these results suggested that AST played key neuroprotective roles on AD via stimulating PI3K/Akt-mTOR pathway-mediated autophagy and autophagic flux. This study revealed a new mechanism of autophagy regulation behind the neuroprotection impact of AST for AD treatment.

Persistent organic pollution in Antarctic marine biota: Level, transport and risk assessment.

Although the Antarctic is considered as a pristine region away from human pollution, traditional and emerging persistent organic pollutants (POPs), such as organochlorine pesticides (OCPs), polychlorinated biphenyls (PCBs), polybrominated diphenyl ethers (PBDEs) and per-/polyfluoroalkyl substances (PFASs), have been constantly detected in the Antarctic, which received global concerns. POPs are persistent and toxic, prone to accumulate in organisms and further pose environmental risks. In order to understand their biogeochemical processes as well as impacts on organisms in the Antarctic, we summarized the research status of POPs in different trophic levels in the Antarctic marine, combining their living habits. We also proposed the future research directions of POPs in the vulnerable Antarctic ecosystem. Researches showed that the Antar-ctic was the region under the lowest pollution level all over the world. However, the types of POPs in Antarctic marine organisms were increasing in the past decades, meaning the area was affected increasingly by the activities inside and/or outside of this area. Scattered research data and different techniques hamper red the elucidation about the mechanism of POPs transport along the food chain. It is urgent to establish long-term monitoring and assessment program on POPs dynamics of Antarctic marine ecosystem.

18F-FDG-PET/CT-guided intensity-modulated radiotherapy for 42 FIGO III/IV ovarian cancer: A retrospective study.

The aim of the present study was to evaluate the curative effect of fludeoxyglucose-positron emission tomography/computed tomography (18F-FDG-PET/CT)-guided intensity-modulated radiotherapy (IMRT) for 42 patients with International Federation of Gynecology and Obstetrics (FIGO) stage III/IV ovarian cancer. Between January 2012 and December 2015, 42 patients with FIGO stage III/IV ovarian cancer who were treated with 18F-FDG-PET/CT-guided IMRT at the Department of Radiation Oncology were analyzed. A total of 21 patients who exhibited recurrence following surgery and 11 patients who were unable to tolerate or rejected surgery received 5-10 cycles of chemotherapy only. A total of 10 patients, who were either older (>70 years) or in poor general health were unable to undergo surgery and only received IMRT. The patients received a total radiation dose of 5,040 cGy (range, 4,500-5,500 cGy), with a dose fraction of 200 cGy/fx, administered a total of 10-14 times, 5 times/week, prior to being rested for half an hour to relocate lesions and undergoing a second round of radiotherapy for 10-14 cycles. The 1-, 2- and 3-year progression-free survival (PFS) rates of the patients were 66.7, 33.3 and 21.4%, respectively, and the median PFS time was 20.3 months. The 1-, 2- and 3-year local control rates of the patients were 90.5, 83.3 and 69.0%, respectively, and the 1-, 2- and 3-year overall survival (OS) rates were 73.8, 64.3 and 52.4%, respectively. According to the results of multivariate analysis using the Cox proportional hazards model, the Karnofsky performance status (KPS) score (1) was the only index associated with prognosis (P<0.003). The study concluded that for patients with advanced ovarian cancer, particularly for patients unable to undergo surgery or chemotherapy, 18F-FDG PET/CT-guided IMRT is a safe and effective treatment method, and it may be considered as an equally effective treatment option. Furthermore, the results of the present study suggested that the KPS score of a patient is the only factor affecting the OS time.

Extract of Ginkgo biloba promotes neuronal regeneration in the hippocampus after exposure to acrylamide.

Previous studies have demonstrated a neuroprotective effect of extract of Ginkgo biloba against neuronal damage, but have mainly focused on antioxidation of extract of Ginkgo biloba. To date, limited studies have determined whether extrasct of Ginkgo biloba has a protective effect on neuronal damage. In the present study, acrylamide and 30, 60, and 120 mg/kg extract of Ginkgo biloba were administered for 4 weeks by gavage to establish mouse models. Our results showed that 30, 60, and 120 mg/kg extract of Ginkgo biloba effectively alleviated the abnormal gait of poisoned mice, and up-regulated protein expression levels of doublecortin (DCX), brain-derived neurotrophic factor, and growth associated protein-43 (GAP-43) in the hippocampus. Simultaneously, DCX- and GAP-43-immunoreactive cells increased. These findings suggest that extract of Ginkgo biloba can mitigate neurotoxicity induced by acrylamide, and thereby promote neuronal regeneration in the hippocampus of acrylamide-treated mice.

Toxic effect of acrylamide on the development of hippocampal neurons of weaning rats.

Although numerous studies have examined the neurotoxicity of acrylamide in adult animals, the effects on neuronal development in the embryonic and lactational periods are largely unknown. Thus, we examined the toxicity of acrylamide on neuronal development in the hippocampus of fetal rats during pregnancy. Sprague-Dawley rats were mated with male rats at a 1:1 ratio. Rats were administered 0, 5, 10 or 20 mg/kg acrylamide intragastrically from embryonic days 6-21. The gait scores were examined in pregnant rats in each group to analyze maternal toxicity. Eight weaning rats from each group were also euthanized on postnatal day 21 for follow-up studies. Nissl staining was used to observe histological change in the hippocampus. Immunohistochemistry was conducted to observe the condition of neurites, including dendrites and axons. Western blot assay was used to measure the expression levels of the specific nerve axon membrane protein, growth associated protein 43, and the presynaptic vesicle membrane specific protein, synaptophysin. The gait scores of gravid rats significantly increased, suggesting that acrylamide induced maternal motor dysfunction. The number of neurons, as well as expression of growth associated protein 43 and synaptophysin, was reduced with increasing acrylamide dose in postnatal day 21 weaning rats. These data suggest that acrylamide exerts dose-dependent toxic effects on the growth and development of hippocampal neurons of weaning rats.

Cortical regulation of striatal projection neurons and interneurons in a Parkinson's disease rat model.

Striatal neurons can be either projection neurons or interneurons, with each type exhibiting distinct susceptibility to various types of brain damage. In this study, 6-hydroxydopamine was injected into the right medial forebrain bundle to induce dopamine depletion, and/or ibotenic acid was injected into the M1 cortex to induce motor cortex lesions. Immunohistochemistry and western blot assay showed that dopaminergic depletion results in significant loss of striatal projection neurons marked by dopamine- and cyclic adenosine monophosphate-regulated phosphoprotein, molecular weight 32 kDa, calbindin, and µ-opioid receptor, while cortical lesions reversed these pathological changes. After dopaminergic deletion, the number of neuropeptide Y-positive striatal interneurons markedly increased, which was also inhibited by cortical lesioning. No noticeable change in the number of parvalbumin-positive interneurons was found in 6-hydroxydopamine-treated rats. Striatal projection neurons and interneurons show different susceptibility to dopaminergic depletion. Further, cortical lesions inhibit striatal dysfunction and damage induced by 6-hydroxydopamine, which provides a new possibility for clinical treatment of Parkinson's disease.

Acrylamide neurotoxicity on the cerebrum of weaning rats.

The mechanism underlying acrylamide-induced neurotoxicity remains controversial. Previous studies have focused on acrylamide-induced toxicity in adult rodents, but neurotoxicity in weaning rats has not been investigated. To explore the neurotoxic effect of acrylamide on the developing brain, weaning rats were gavaged with 0, 5, 15, and 30 mg/kg acrylamide for 4 consecutive weeks. No obvious neurotoxicity was observed in weaning rats in the low-dose acrylamide group (5 mg/kg). However, rats from the moderate- and high-dose acrylamide groups (15 and 30 mg/kg) had an abnormal gait. Furthermore, biochemical tests in these rats demonstrated that glutamate concentration was significantly reduced, and γ-aminobutyric acid content was significantly increased and was dependent on acrylamide dose. Immunohistochemical staining showed that in the cerebral cortex, γ-aminobutyric acid, glutamic acid decarboxylase and glial fibrillary acidic protein expression increased remarkably in the moderate- and high-dose acrylamide groups. These results indicate that in weaning rats, acrylamide is positively associated with neurotoxicity in a dose-dependent manner, which may correlate with upregulation of γ-aminobutyric acid and subsequent neuronal degeneration after the initial acrylamide exposure.

Volatilization behaviors of diesel oil from the soils.

The volatilization of diesel oil, Shengli crude oil and 90 # gasoline on glass surface of petri dishes were conducted at the ambient temperature of 25 degrees C. Diesel oil evaporates in a power manner, where the loss of mass is approximately power with time. 90 # gasoline evaporates in a logarithmic with time. Where as the volatilization of Shengli crude oil fit either the logarithmic or power equation after different time, and has similar R2. And the effects of soil type and diesel oil and water content on volatilization behavior in unsaturated soil were studied in this paper. Diesel oil and water content in the soils play a large role in volatilization from soils. Appropriate water helps the wicking action but too much water stops it. The wicking action behaves differently in four different types of soils in the same volatilization experiment of 18% diesel oil content and air-dry condition.

EPO-dependent activation of PI3K/Akt/FoxO3a signalling mediates neuroprotection in in vitro and in vivo models of Parkinson's disease.

Erythropoietin (EPO) may become a potential therapeutic candidate for the treatment of the neurodegenerative disorder -- Parkinson's disease (PD), since EPO has been found to prevent neuron apoptosis through the activation of cell survival signalling. However, the underlying mechanisms of how EPO exerts its neuroprotective effect are not fully elucidated. Here we investigated the mechanism by which EPO suppressed 6-hydroxydopamine (6-OHDA)-induced neuron death in in vitro and in vivo models of PD. EPO knockdown conferred 6-OHDA-induced cytotoxicity. This effect was reversed by EPO administration. Treatment of PC12 cells with EPO greatly diminished the toxicity induced by 6-OHDA in a dose- and time-dependent manner. EPO effectively reduced apoptosis of striatal neurons and induced a significant improvement on the neurological function score in the rat models of PD. Furthermore, EPO increased the expression of phosphorylated Akt and phosphorylated FoxO3a, and abrogated the 6-OHDA-induced dysregulation of Bcl-2, Bax and Caspase-3 in PC12 cells and in striatal neurons. Meanwhile, the EPO-dependent neuroprotection was notably reversed by pretreatment with LY294002, a specific inhibitor of phosphatidylinositol 3-kinase (PI3K). Our data suggest that PI3K/Akt/FoxO3a signalling pathway may be a possible mechanism involved in the neuroprotective effect of EPO in PD.