Transcriptomics analysis and fed-batch regulation of high astaxanthin-producing Phaffia rhodozyma/Xanthophyllomyces dendrorhous obtained through adaptive laboratory evolution.

Astaxanthin has high utilization value in functional food because of its strong antioxidant capacity. However, the astaxanthin content of Phaffia rhodozyma is relatively low. Adaptive laboratory evolution is an excellent method to obtain high-yield strains. TiO2 is a good inducer of oxidative stress. In this study, different concentrations of TiO2 were used to domesticate P. rhodozyma, and at a concentration of 1000 mg/L of TiO2 for 105 days, the optimal strain JMU-ALE105 for astaxanthin production was obtained. After fermentation, the astaxanthin content reached 6.50 mg/g, which was 41.61% higher than that of the original strain. The ALE105 strain was fermented by batch and fed-batch, and the astaxanthin content reached 6.81 mg/g. Transcriptomics analysis showed that the astaxanthin synthesis pathway, and fatty acid, pyruvate, and nitrogen metabolism pathway of the ALE105 strain were significantly upregulated. Based on the nitrogen metabolism pathway, the nitrogen source was adjusted by ammonium sulphate fed-batch fermentation, which increased the astaxanthin content, reaching 8.36 mg/g. This study provides a technical basis and theoretical research for promoting industrialization of astaxanthin production of P. rhodozyma. ONE-SENTENCE SUMMARY: A high-yield astaxanthin strain (ALE105) was obtained through TiO2 domestication, and its metabolic mechanism was analysed by transcriptomics, which combined with nitrogen source regulation to further improve astaxanthin yield.

Is lymphatic invasion of microrectal neuroendocrine tumors an incidental event?: A case report.

BACKGROUND: A rectal neuroendocrine tumor (rNET) is a malignant tumor originating from neuroendocrine cells. Currently, tumor size is the primary basis for assessing tumor risk. CASE SUMMARY: This article reports the case of a 46-year-old male patient who underwent a colonoscopy that found a 3 mm rectal polypoid bulge. The pathological examination of a sample collected with biopsy forceps revealed a neuroendocrine tumor. Further endoscopic submucosal dissection rescue therapy was used. The presence of lymphatic vessels indicated that the tumor had infiltrated the negative resection margin. The lesion was located in the distal rectum near the anal canal. Therefore, to ensure the patient's quality of life, follow-up observation was conducted after full communication with the patient. No tumor recurrence or distant metastasis has been found during the 13-mo follow-up after surgery. CONCLUSION: Despite the presence of lymphatic invasion and extremely small diameter rNETs in our case, this phenomenon may not imply a higher risk of distant lymph node and organ metastasis.

Angiotensin receptor antagonist losartan improves endothelial function of epicardial coronary arteries in patients with essential hypertension.

BACKGROUND: Angiotensin II can impair endothelial function, which is mediated by the angiotensin II type 1 receptor subtype. HYPOTHESIS: The study sought to determine whether treatment with the angiotensin II type 1 receptor antagonist losartan would restore the normal dilation of the left main coronary artery (LMCA) by cold pressor test in patients with essential hypertension, as shown by echocardiography. METHODS: The study population included 30 patients with mild to moderate essential hypertension and 30 matched healthy subjects. Measurements of the cold pressor test-induced and nitroglycerin-induced changes in LMCA diameter by echocardiography were performed at the end of the washout period and after 12 weeks of losartan administration. RESULTS: The percent change in LMCA diameter induced by the cold pressor test in hypertensive patients (-3.5 +/- 8.8%) was significantly lower than that in control subjects (10.2 +/- 3.7%, p<0.0001). After losartan treatment, the percent change (13.9 +/- 8.4%) was significantly higher than that before losartan treatment (-3.5 +/- 8.8%, p < 0.0001), but not significandy different between the 17 hypertensive patients with satisfactory control of blood pressure (13.8 +/- 9.1%) and the 13 hypertensive patients without satisfactory control of blood pressure (14.0 +/- 7.7%, p = 0.9). Losartan treatment in patients with essential hypertension did not modify the percent change in LMCA diameter caused by sublingual administration of nitroglycerin (23.2 +/- 14.0% vs. 27.3 +/- 13.7%, p = 0.2). CONCLUSIONS: This study demonstrates that treatment with losartan normalized response of the LMCA to the cold pressor test in patients with mild to moderate essential hypertension and that this effect is not dependent on the reduction of blood pressure.

Effects of the angiotensin receptor antagonist losartan on the response of the left main coronary artery to cold pressor test in patients with essential hypertension as assessed by echocardiography.

BACKGROUND: Angiotensin II can impair endothelial function, which is mediated by the angiotensin II type 1 receptor subtype. OBJECTIVE: To test the hypothesis that treatment with the angiotensin II type 1 receptor antagonist losartan would restore the normal dilation of the left main coronary artery to the cold pressor test in patients with essential hypertension, as assessed by echocardiography. PATIENTS AND METHODS: The study population included 24 patients with mild to moderate essential hypertension and 24 matched, healthy subjects. The cold pressor test-induced and nitroglycerin-induced changes in the left main coronary artery diameter were measured by echocardiography at the end of the washout period and after 12 weeks of losartan administration. RESULTS: The percentage change in the left main coronary artery diameter induced by the cold pressor test in patients with hypertension (-4.3 8.7%) was significantly lower than that in control subjects (10.5 3.9%, P<0.0001). The percentage change in the left main coronary artery diameter induced by the cold pressor test in patients with essential hypertension after losartan treatment (13.7 8.0%) was significantly higher than that before losartan treatment (-4.3 8.7%, P<0.0001). The percentage change in the left main coronary artery diameter induced by the cold pressor test after losartan treatment was not significantly different between the 14 patients with hypertension who had satisfactory control of blood pressure (14.1 8.8%) and the 10 patients with hypertension who did not have satisfactory control of blood pressure (13.1 7.0, P=0.8). Losartan treatment in patients with essential hypertension did not modify the percentage change in the left main coronary artery diameter caused by sublingual administration of nitroglycerin (23.2 14.4% versus 27.2 13.5, P=0.2). CONCLUSIONS: The present study demonstrates that treatment with the angiotensin II type 1 receptor antagonist losartan normalized the response of the left main coronary artery to the cold pressor test in patients with mild to moderate essential hypertension, and that this effect is not dependent on the reduction of blood pressure.