Ketones,phenols and their derivatives(referred as KPs) were extracted from natural plants with ultrasonic-organic solvent technology.Stable porphyrin compounds,HPs,were made from the haematochrome extracted from fresh animal blood with acidic acetone.And then a complex biochemical agent was prepared.By taking tea powder as a carrier,a dual filter was made and applied in filter cigarette manufacturing.The test results showed that: comparing with the control, the contents of polycyclic aromatic hydrocarbons,tobacco specific N-nitrosoamines,free radicals,aromatic amines,and other harmful components in mainstream smoke of cigarettes with the dual filter were reduced significantly.The mechanism of harmful component reducing of complex biochemical agent was also discussed.
Abstract Serum Amyloid A (SAA) is an acute-phase protein, released predominantly from the liver during large scale inflammation. High SAA levels, up to 1000 times normal, are also associated with autoimmune conditions like Rheumatoid Arthritis (RA). SAA is found in very high levels in the arthritic joints of patients, along with a high concentration of certain subsets of T lymphocytes, notably helper T cell type 1 (Th1). The marker for Th1 cells is production of the cytokine interferon gamma (IFNγ). The purpose of this study is to determine if SAA stimulation of murine T cells causes Th1 differentiation. CD4+ T-cells isolated from the spleens of wild type mice have been stimulated in vitro with SAA protein. IFNγ production was measured and compared to that of the known inducer of Th1 cells, interleukin-12 (IL-12). Indeed, SAA stimulation induced IFNγ production with levels as high as 22,088 pg/mL, which is comparable to the 20,237 pg/mL induced by IL-12. Our data also shows that SAA and IL-12 can co-stimulate T cells and result in even higher levels of IFNγ secretion. Future experiments will confirm Th1 differentiation by detecting cell surface markers with flow cytometry and will also investigate the intracellular actions of SAA stimulation. These results suggest that SAA and Th1 cells are found together in arthritic joints because SAA induces this T-cell subset’s production, and is perhaps a missing link in our understanding of RA.
Objective To elucidate the risk factors in the development of hepatocellular carcinoma in the villages with high and relatively low mortality of hepatocellular carcinoma in the minority nationality of Yaos in Guangxi province.Methods Epidemiology method was applied to investigate the incidence of hepatocellular carcinoma,infection and replication of hepatitis B and C virus,living environment of the subjects in the villages with high and relatively low mortality of hepatocellular carcinoma discovered recently in the minority nationality of Yaos in Guangxi province.Results The mortality of hepatocellular carcinoma discovered recently had a rude mortality with 104.77/100000 and 55.76/100000 in the higher mortality village and the relative lower mortality village respectively.There was no significant difference of the mortality between the two villages(P0.05);The positive rates of HBsAg and HBVDNA were 17.8%(11/62),12.9%(8/62) and 9.4%(10/107),4.7%(5/107) respectively.No significant difference of HBsAg positive rate between the two villages could be seen(χ2=2.54,P=0.11),while there was a significant difference of HBVDNA positive rate between the two villages(χ2=3.75,P=0.05).The positive rate of anti-HBs was 53.2%(33/62)and 60.7%(65/107)respectively(χ2=0.91,P=0.34).People living in the higher mortality village had pond water as living water 10 years ago.No HCV infection was found in the two villages.Conclusions The risk factors in the development of hepatocellular carcinoma in the high mortality area discovered recently in the national minority of Yaos in Guangxi province are hepatitis B virus infection,especially the replication of HBVDNA,pond water drinking and genetics factor.Aflatoxin taking and hepatitis C virus infection play no role in the development of hepatocellular carcinoma in these villages.
This article reported the clinical characteristics and SRD5A2 gene mutation pattern of a child with steroid 5-α reductase type 2 deficiency. The 2-month-old boy showed hypospadias and short penis shortly after birth. DNA was extracted from the peripheral blood of the child and his parents. The endocrine disease-related genes were captured and sequenced by high-throughput sequencing technology, and the family DNA samples were verified by Sanger sequencing. The results showed that c.680G>A(p.R227Q) and c.608G>A(p.G203D) compound heterozygous mutations existed in the SRD5A2 gene of the child. The c.680G>A mutation inherited from his father, which was a known pathogenic mutation. The c.608G>A mutation originated from his mother, which was a novel mutation discovered in this study. These results provide molecular evidence for the etiological diagnosis of the child and genetic counseling for the family, as well as extend the mutation spectrum of SRD5A2 gene.
To carry out cyto- and molecular genetic analysis for a fetus with a ring chromosome identified through non-invasive prenatal testing (NIPT).A pregnant woman presented at the Shengjing Hospital Affiliated to China Medical University on May 11, 2021 was selected as the study subject. Maternal peripheral blood sample was screened by NIPT, and G-banded chromosomal karyotyping was carried out on amniotic fluid and peripheral blood samples from the couple. The fetus and the pregnant woman were also subjected to genomic copy number variation sequencing (CNV-seq), chromosomal microarray analysis (CMA), and fluorescence in situ hybridization (FISH) assay.NIPT result suggested that the fetus had monomeric mosaicism or fragment deletion on chromosome 13. G banded chromosomal analysis showed that both the fetus and its mother had a karyotype of 47,XX,der(13)(pter→p11::q22→q10),+r(13)(::p10::q22→qter::), whilst her husband had a normal karyotype. FISH has verified the above results. No abnormality was detected with CNV-seq and CMA in both the fetus and the pregnant woman.The ring chromosome 13 in the fetus has derived from its mother without any deletion, duplication and mosaicism. Both the fetus and the pregnant woman were phenotypically normal.
AIM: To study the effect of glucose-insulin-potassium(GIK) on changes of dog myocardial cells after ischemia-reperfusion injury following acute myocardial ischemia/reperfusion(MI/R) and to explore the role of insulin in the protective effects of GIK on myocardium.METHODS: In anesthetized open-chest dogs,the left anterior descending coronary artery(LAD) was partially occluded(80% reduction in its blood flow) for 50 min and reperfused for 4 h.Dogs were randomly divided into three groups: GIK,GK and saline.All treatments began at 5 min before reperfusion [infused at 2 ml/(kg·h),i.v.] and continued during the 4-h reperfusion.The ratio of necrosis area was determined.Myocardial infarction was determined by the ultrastructure of ischemic myocardium at the end of the reperfusion.RESULTS: The ratio of myocardial necrosis showed attenuation in GIK group [(5.2±0.8)% vs.saline(9.4±0.8)%,P0.05],but no reduction was observed in myocardial infarct size in the GK group [(8.5±0.9)% vs.saline(9.4±0.8)%].Compared with saline,GK had no significant effects on the ultrastructure of ischemic myocardium,whereas GIK had significant effects on the ultrastructure of ischemic myocardium.CONCLUSION: GIK exerts some protective effects on myocardium by alleviating ultrastructural injury of myocardium.Insulin may play a leading role in the actions of GIK.
Abstract Background Citrullinemia type I (CTLN1) is a rare urea cycle disorder (UCD) with few adult cases described so far. Diagnosis of late-onset CTLN1 is difficult, and delayed treatment may increase the risk of severe hyperammonemia. Pregnancy is an important risk factor for women with CTLN1. However, the clinical manifestations of CTLN1 in a pregnant woman may be mistaken for pregnancy side effects and ultimately delay a timely diagnosis. Case presentation A 34-year-old woman developed vomiting and disturbance of consciousness after 12 weeks of gestation. A blood test showed hyperammonemia (454 μg/dL) with normal liver function tests. She fell into a deep coma, and her serum ammonia level increased to 800 μg/dL. Continuous renal replacement therapy (CRRT) was administered as a diagnostic treatment for UCD and serum ammonia. This patient’s case was complicated by co-infection; her dependents decided to withdraw life support and the patient died. She was diagnosed with CTLN1 by analyses of plasma amino acids, urinary orotic acid, and second-generation gene sequencing. Discussion and conclusion When a patient displays symptoms of emesis and disturbance of consciousness in early pregnancy, blood ammonia should be monitored, and UCD should be considered, particularly for patients with hyperammonemia in the absence of severe liver function abnormalities.
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