Numerous studies have indicated that organic fertilizers (OFer) might contain heavy metals (HMs) that present health risks to organic farmers (OFar). This study compared the concentrations of six HMs (Zn, Ni, Cd, Cu, Pb, Cr) in the blood of two distinct groups of farmers: 30 OFar from a designated organic area in eastern Taiwan, and 74 conventional farmers (CFar) from neighboring non-organic designated regions. The findings revealed that the OFar exhibited higher levels of Zn (1202.70 ± 188.74 μg/L), Cr (0.20 ± 0.09 μg/L), and Ni (2.14 ± 1.48 μg/L) in their blood compared to the CFar (988.40 ± 163.16 μg/L, 0.18 ± 0.15 μg/L, and 0.77 ± 1.23 μg/L), respectively. The disparities in Zn, Cr, and Ni levels were measured at 214.3 μg/L, 0.02 μg/L, and 1.37 μg/L, respectively. Furthermore, among the OFar, those who utilized green manures (GM) displayed significantly elevated blood levels of Zn (1279.93 ± 156.30 μg/L), Cr (0.24 ± 0.11 μg/L), and Ni (1.94 ± 1.38 μg/L) compared to individuals who exclusively employed chemical fertilizers (CFer) (975.42 ± 165.35 μg/L, 0.19 ± 0.16 μg/L, and 0.74 ± 1.20 μg/L), respectively. The differences in Zn, Cr, and Ni levels were measured at 304.51 μg/L, 0.05 μg/L, and 1.20 μg/L, respectively. As a result, OFar should be careful in choosing OFer and avoid those that may have heavy metal contamination.

Background: Liver regeneration is dependent on the proliferation of hepatocytes. Hepatic progenitorcells are intra-hepatic precursor cells capable of differentiating into hepatocytes or biliary cells.Although liver progenitor cell proliferation during the regenerative process has been observed in animalmodels of severe liver injury, it has never been observed in vivo in humans because it is unethicalto take multiple biopsy specimens for the purpose of studying the proliferation of liver progenitorcells and the roles they play in liver regeneration. Associating liver partition and portal vein ligationfor staged hepatectomy (ALPPS) is a staged procedure for inducing remnant liver hypertrophy sothat major hepatectomy can be performed safely. This staged procedure allows for liver biopsyspecimens to be taken before and after the liver begins to regenerate. Case presentation: The liverprogenitor cell proliferation is observed in a patient undergoing ALPPS for a metastatic hepatictumour. Liver biopsy is acquired before and after ALPPS for the calculation of average number ofliver progenitor cell under high magnification examination by stain of immunomarkers. This is thefirst in vivo evidence of growing liver progenitor cells demonstrated in a regenerating human liver.

OBJECTIVE: The purpose of this study was to quantify lesions on chest radiographs in patients with severe acute respiratory syndrome (SARS) and analyze the severity of the lesions with clinical parameters. MATERIALS AND METHODS: Two experienced radiologists reviewed chest radiographs of 28 patients with SARS. Each lung was divided into upper, middle, and lower zones. A SARS-related lesion in each zone was scored using a four-point scale: zero to three. The mean and maximal radiographic scores were analyzed statistically to determine if the scorings were related to the laboratory data and clinical course. RESULTS: Forward stepwise multiple linear regression showed that the mean radiographic score correlated most significantly with the number of hospitalized days (p < 0.001). The second most significant factor was the absolute lymphocyte count (p < 0.001) and the third most significant factor was the number of days of intubation (p = 0.025). The maximal radiographic score correlated best with the percentage of lymphocytes in a leukocyte count (p < 0.001), while the second most significant factor was the number of hospitalized days (p < 0.001) and the third most significant factor was the absolute lymphocyte count (p = 0.013). The mean radiographic scores of the patients who died, with comorbidities and without a comorbidity were 11.1, 6.3 and 2.9, respectively (p = 0.032). The corresponding value for maximal radiographic scores were 17.7, 9.7 and 6.0, respectively (p = 0.033). CONCLUSION: The severity of abnormalities quantified on chest radiographs in patients with SARS correlates with the clinical parameters.
Adolescent ; Adult ; Aged ; Aged, 80 and over ; Biological Markers/blood ; Blood Gas Analysis/statistics & numerical data ; Female ; Humans ; Intubation, Intratracheal/statistics & numerical data ; Length of Stay ; Lung/*radiography ; Lymphocyte Count/statistics & numerical data ; Male ; Middle Aged ; Observer Variation ; Predictive Value of Tests ; Prognosis ; Retrospective Studies ; Severe Acute Respiratory Syndrome/blood/*diagnosis/mortality ; Severity of Illness Index ; Survival Analysis

Angiotensin II Type 1 Receptor Blockers ; administration & dosage ; Animals ; Coronary Angiography ; Coronary Restenosis ; prevention & control ; Coronary Vessels ; pathology ; Drug Delivery Systems ; Immunohistochemistry ; Rabbits ; Receptor, Angiotensin, Type 1 ; analysis ; Receptor, Angiotensin, Type 2 ; analysis ; genetics ; physiology ; Reverse Transcriptase Polymerase Chain Reaction ; Stents ; Tetrazoles ; administration & dosage ; Valine ; administration & dosage ; analogs & derivatives ; Valsartan

OBJECTIVETo assess the effect of valsartan eluting-stents on restenosis and collagen deposition in neointima hyperplasia in rabbits.

METHODSValsartan eluting-stents and the carrier eluting-stents were made with patented multi-layers coating techniques. Bare stents (n = 8), carrier eluting-stents (n = 8) and valsartan eluting-stents (n = 10) were implanted into rabbit abdominal aortas, respectively. Quantitive angiography (QA) was performed before, immediately post and 3 months after stents implantations to determine the diameter of aortas. Rabbits were killed 3 months post stents implantation and the cross sections of the stented vessels were analyzed for neointimal formation: luminal area (LA), neointimal area (NIA), inner elastic lumina area (IELA), the maximal inner-membrane thickness (MIT) and percent stenosis. MASSON and picrosirius red staining were performed to observe the collagen deposition in neointima analyzed.

RESULTSThe mean aortic diameters measured by QA at different time points were similar between the groups. LA was significantly larger (5 016 269 microm(2) +/- 207,934 microm(2) vs. 4,345,548 microm(2) +/- 125,822 microm(2) and 4,302,061 microm(2) +/- 167,952 microm(2), P < 0.01 vs. valsartan stents) while NIA (441,577 microm(2) +/- 74,099 microm(2) vs. 1,119,635 microm(2) +/- 163,503 microm(2) and 1,135,636 microm(2) +/- 136,555 microm(2)) and MIT (116 microm +/- 12 microm vs. 240 microm +/- 30 microm and 192 microm +/- 21 microm) as well as percent stenosis (8% +/- 2% vs. 20% +/- 2% and 21% +/- 2%) were significantly reduced in valsartan eluting-stents group compared to bare and carrier stents groups. MASSON and picrosirius red staining revealed rich type III collagen deposition in neointima and spare type I collagen patched around stents struts in bare and carrier stents groups and collagen deposition was rarely seen in neointima and stents struts in valsartan eluting-stents group.

CONCLUSIONValsartan eluting-stents inhibited neointimal hyperplasia by decreasing collagen deposition.

Animals ; Collagen ; metabolism ; Coronary Restenosis ; metabolism ; pathology ; therapy ; Coronary Vessels ; pathology ; Drug-Eluting Stents ; Female ; Graft Occlusion, Vascular ; metabolism ; pathology ; Hyperplasia ; Male ; Rabbits ; Tetrazoles ; therapeutic use ; Tunica Intima ; pathology ; Valine ; analogs & derivatives ; therapeutic use ; Valsartan

Background/Aims: Chronic hepatitis C (CHC) patients who failed antiviral therapy are at increased risk for hepatocellular carcinoma (HCC). This study assessed the potential role of metformin and statins, medications for diabetes mellitus (DM) and hyperlipidemia (HLP), in reducing HCC risk among these patients. Methods: We included CHC patients from the T-COACH study who failed antiviral therapy. We tracked the onset of HCC 1.5 years post-therapy by linking to Taiwan’s cancer registry data from 2003 to 2019. We accounted for death and liver transplantation as competing risks and employed Gray’s cumulative incidence and Cox subdistribution hazards models to analyze HCC development. Results: Out of 2,779 patients, 480 (17.3%) developed HCC post-therapy. DM patients not using metformin had a 51% increased risk of HCC compared to non-DM patients, while HLP patients on statins had a 50% reduced risk compared to those without HLP. The 5-year HCC incidence was significantly higher for metformin non-users (16.5%) versus non-DM patients (11.3%; adjusted sub-distribution hazard ratio [aSHR]=1.51; P=0.007) and metformin users (3.1%; aSHR=1.59; P=0.022). Statin use in HLP patients correlated with a lower HCC risk (3.8%) compared to non-HLP patients (12.5%; aSHR=0.50; P<0.001). Notably, the increased HCC risk associated with non-use of metformin was primarily seen in non-cirrhotic patients, whereas statins decreased HCC risk in both cirrhotic and non-cirrhotic patients. Conclusions Metformin and statins may have a chemopreventive effect against HCC in CHC patients who failed antiviral therapy. These results support the need for personalized preventive strategies in managing HCC risk.