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1.
本文根据激光,生物学的特点以及两者相互作用的机理和实验结果,初步探讨了激光与生物学的交叉学科内某些因素的相互关系。作了激光波长对鱼类生长速率,鱼类受精卵孵化率,鱼类胚胎畸变的影响和激光辐照剂量对鱼类生长速率的影响实验。  相似文献   

2.
激光及激光生物学发展概况   总被引:11,自引:1,他引:10  
本文介绍了激光、激光应用和激光生物学发展概况  相似文献   

3.
本文研究表明,低剂量的激光可以提高精子的活力和呼吸,两者之间存在有强的正相关关系,说明激光辐照精子后,促进了精子的呼吸,合成了较多的ATL提高了精子的活力。  相似文献   

4.
朱延彬  马俊富 《激光生物学报》1994,3(3):516-519,528
本广简介了我们研制成功的两种激光微束系统的设计特点,文中并综述了激光微束技术的应用前景。  相似文献   

5.
本实验采用新技术激光辐射种蛋。结果表明,一定剂量的激光能显著提高种蛋的孵化率(6.68% ̄13.26%),雏鸡的体重和生活力;同时还对激光的作用机理作了初步探讨。  相似文献   

6.
氦氖激光对种公牛精子生物学效应的研究   总被引:1,自引:0,他引:1  
岳文斌  张渊 《激光生物学报》1992,1(3):115-116,111
本文采用氦氖激光辐射种公牛的精液,发现低剂量的氖氦激光可以提高精子的活力,存活时间和呼吸强度,降低精子的畸形率,并对其机理作了探讨。  相似文献   

7.
李挺 《蛇志》1992,4(4):28-33
自1960年 Maiman 研制成第一台红宝石激光器以后,由于激光以强大集中的能量,不同波长对组织作用的特性及光导纤维的传输等等,赋予了医学一种潜在的革命,因而,六十年代从眼科、皮肤科、外科、妇科及肿瘤科扩展到医学各个领域,包括基础及诊断预防医学.近十余年来由于激光器迅速发展,光纤传输的方便,以及激光——组织间关系的研究成果,使得激光医学更是突飞猛进,加之激光工程技术人员与医务人员紧密合作,为发展激光医学做出了更大的贡献。由于激光医疗极为广泛,这里仅就激光在普外的应用作一文献复习,综述如下:激光应用于普外科在外科领域为最早之学科.1963年开始用较大功率脉冲激光来汔化和烧灼表浅肿瘤,由于存在“飞溅”现象和压力效应而暂停.  相似文献   

8.
本文引用等效模型,对激光消融过程进行了推导与计算,和实验结果比较表明,所得公式与实验结果能较好相符,可用于描述紫外激光消融过程。  相似文献   

9.
激光技术在农产品质量检测中的研究进展   总被引:7,自引:0,他引:7  
近年来激光在农业领域得到广泛的应用和研究,其中的一个最新进展是将激光技术应用于农产品内部品质和安全性检测。本文介绍了农产品质量检测中的几种激光技术,包括应用激光的吸收与反射技术来检测农产品糖酸度、质地、PH值、成熟度、干物质等;应用激光诱导荧光技术来检测农产品的农药残留、叶绿素、成熟度;应用激光拉曼光谱技术来检测农产品水果损伤、农药残留。对农产品激光检测的未来发展趋势进行了探讨和展望。  相似文献   

10.
CO2激光辐射黄瓜种子对种子活力影响的研究   总被引:6,自引:1,他引:5  
采用功率密度为898mw/cm^2的CO2激光对黄瓜子种子进行不同时间的照射处理,其结果表明,3s-7s均有不同程度的刺激效应,30s以上出现了不同程度的抑制作用和畸形芽,其中的90s组已达到了半致死剂量。  相似文献   

11.
Vitamins and brain development.   总被引:1,自引:0,他引:1  
Effects of deficiency of vitamins on early development of brain have been reviewed. Unusual developmental problems in neurogenesis specific for the brain and impairment of its functional capacities due to vitamin deficiency have been discussed. The species-specific "critical periods" in development of various systems have been mentioned. Indices such as reflex activity, locomotion, special senses, cognition and adaptive behavior were used for assessing brain maturation in experimental models and humans. Significant examples include brain anomalies in humans and other mammals caused by retinoid excess or deficit; increase in calbindin D28K, a vitamin D dependent calcium-binding protein during postnatal period in rat; hydrocephalus and exencephaly in prenatal rats and subarachnoidal or intracerebral hemorrhage in infants caused by vitamin E deficiency. Peripheral neuropathic lesions leading to infantile beriberi is caused by thiamine deficiency. Impaired growth in retinal layers leading to delay in maturation of electroretinogram and depth-perception in postnatal rats occur due to pyridoxine deficiency. Infants of severely vitamin B12 deficient mothers show abnormalities in behavior involving basal ganglia and pyramidal tract. Folic acid deficiency results in delayed maturation of the basic electroencepalographic patterns. In addition, vitamin-interactions leading to developmental errors have been pointed out. Vitamin B6 deficiency impairs vitamin B12 absorption and biotin deficiency may be aggravated by pantothenic acid deficiency. Vitamin C deficiency resulting in impaired metabolism may produce symptoms of deficiency of folic acid. Another characteristic examples is that iron absorption from dietary sources is dependent on ascorbic acid.  相似文献   

12.
The most potent corticosteroids are 11beta-hydroxylated compounds. In humans, two cytochrome P450 isoenzymes with 11beta-hydroxylase activity, catalysing the biosynthesis of cortisol and aldosterone, are present in the adrenal cortex. CYP11B1, the gene encoding 11beta-hydroxylase (P450c11), is expressed on high levels in the zona fasciculata and is regulated by ACTH. CYP11B2, the gene encoding aldosterone synthase (P450c11Aldo), is expressed in the zona glomerulosa under primary control of the renin-angiotensin system. Aldosterone synthase has 11beta-hydroxylase activity as well as 18-hydroxylase activity and 18-oxidase activity. The substrate for CYP11B2 is 11-deoxycorticosterone, that of CYP11B1 is 11-deoxycortisol. Mutations in CYP11B1 cause congenital adrenal hyperplasia (CAH) due to 11beta-hydroxylase deficiency. This disorder is characterized by androgen excess and hypertension. Mutations in CYP11B2 cause congenital hypoaldosteronism (aldosterone synthase deficiency) which is characterized by life-threatening salt loss, failure to thrive, hyponatraemia and hyperkalaemia in early infancy. Both disorders have an autosomal recessive inheritance. Classical and nonclassical forms of 11beta-hydroxylase deficiency can be distinguished. Studies in heterozygotes for classical 11beta-hydroxylase deficiency show inconsistent results with no or only mild hormonal abnormalities (elevated plasma levels of 11-deoxycortisol after ACTH stimulation). In infants with congenital hypoaldosteronism, a comparable frequency of 18-hydroxylase deficiency (aldosterone synthase deficiency type I) and of 18-oxidase deficiency (aldosterone synthase deficiency type II) can be found. Molecular genetic studies of the CYP11B1 and CYP11B2 genes in 11beta-hydroxylase deficiency or aldosterone synthase deficiency have led to the identification of several mutations. Transfection experiments showed loss of enzyme activity in vitro. In some of the patients with 18-oxidase deficiency (aldosterone synthase deficiency type II) no mutations in the CYP11B2 gene were identified. Refined methods for steroid determination are the basis for the diagnosis of inborn errors of steroidogenesis. Molecular genetic studies are complementary; on the one hand, they have practical importance for the prenatal diagnosis of virilizing CAH forms and on the other hand, they are of theoretical importance in terms of our understanding of the functioning of cytochrome P450 enzymes. Copyrightz1999S.KargerAG, Basel  相似文献   

13.
We studied the prevalence of zinc deficiency in patients who were hospitalised in a geriatric ward and its association with risk factors for this deficiency and the possible symptoms. The serum zinc level was measured from 45 consecutive admissions to a geriatric ward and patient characteristics were collected. A peer group of healthy subjects originating from a population survey was used as a control group. The serum zinc measured in the admitted patients was significantly lower than the reference value for adults (65.8% had a lowered zinc level) and the serum zinc for healthy elderly. There was no association found with possible causes of zinc deficiency. In an univariate analysis lethargy was the only significant association to zinc deficiency. There was a reverse relationship between the sum of the number of present symptoms and the zinc proportion A lower zinc level is associated with symptoms of zinc deficiency. As more symptoms appear the probability of zinc deficiency is greater. The importance for the clinical practice based on present knowledge is discussed.  相似文献   

14.
The vitamin D and K deficiency was studied for its effect on creatine kinase, phosphorylase and alkaline phosphatase activity of rat kidneys and intestinal mucosa. The results show that creatine kinase and phosphorylase activity of kidneys varies depending on the content of these vitamins, e.g. it is activated with vitamin D depletion irrespective of the vitamin K status and remains unchanged with the deficiency of vitamin K alone. In this case the vitamin D deficiency affects kidney phosphorylase and intestinal mucosa differently. Data obtained and those available in literature permit suggesting that the deficiency of the same vitamin may exert a different action on the activity of isoforms of such enzymes as creatine kinase and phosphorylase.  相似文献   

15.
Vitamin E and neurologic function in man   总被引:1,自引:0,他引:1  
Despite the well-known detrimental effect of vitamin E deficiency on the nervous system of many experimental animal models for decades, only over the past decade has vitamin E become recognized as essential for the maintenance of the structure and function of the human nervous system. This discovery of the neurologic role of vitamin E in man is due primarily to the identification of a degenerative neurologic syndrome in children and adults with chronic vitamin E deficiency caused by gastrointestinal diseases impairing fat and vitamin E absorption. A compelling body of clinical, neuropathologic, and therapeutic response evidence conclusively demonstrates that vitamin E deficiency is responsible for the neurologic disorder seen in such patients. In addition, an inborn error in vitamin E metabolism, the Isolated Vitamin E Deficiency Syndrome, causes vitamin E deficiency and similar neurologic degeneration in the absence of fat malabsorption. Guidelines for the evaluation and treatment of vitamin E deficiency in relevant clinical circumstances are provided. The possible role of vitamin E in treating other neurologic diseases is discussed.  相似文献   

16.
High frequencies of both thalassemia trait (5.2%) and glucose 6-phosphate dehydrogenase (G6PD) deficiency for only males (1.3%) have been observed in the Calabrian population. The G6PD activity measurement was carried out on 1239 samples of whole blood from Calabrian subjects of both sexes (age range 10-55) by a differential pH-metry technique which was quite suitable to determine the G6PD deficiency in mass screenings. The analyzed subjects showed: only the thalassemia trait; or only the G6PD deficiency; or only the total iron serum deficiency; or G6PD deficiency associated with the thalassemia trait or with the total iron serum deficiency. The G6PD heterozygous subjects have an enzymatic activity which is masked by both the thalassemia trait and the total iron serum deficiency. In a population showing high frequencies of both thalassemia trait and G6PD deficiency, the comparison of G6PD activity of heterozygous subjects also affected with the thalassemia trait is more reliable if referred to the enzymatic activity of the carriers of the latter inherited anomaly rather than to G6PD activity of normal subjects.  相似文献   

17.
E R Jaffé 《Blood cells》1986,12(1):81-90
Recessively inherited NADH-cytochrome B5 reductase deficiency, when present in the homozygous or doubly heterozygous form, is manifested by two different clinical presentations, depending on the nature and cellular distribution of the mutant enzyme. The observations supporting a clinical and biochemical classification of enzymopenic hereditary methemoglobinemia are summarized. Type I, with deficiency demonstrable only in the erythrocytes, presents as uncomplicated, benign methemoglobinemia. Type II, generalized cytochrome B5 deficiency demonstrable in all of the tissues that have been examined, is accompanied by severe, lethal, progressive neurological disability, in addition to methemoglobinemia. Type III deficiency is limited to hematopoietic cells and resembles Type I clinically. Type IV, also clinically like Type I, is associated with deficiency of the cofactor, cytochrome B5. Except for Type IV, the different types appear to be the result of mutations in paired alleles of a gene on chromosome 22 that affect the catalytic activity or stability of the cytochrome B5 reductase.  相似文献   

18.
A wide variety of symptoms is associated with Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection, and these symptoms can overlap with other conditions and diseases. Knowing the distribution of symptoms across diseases and individuals can support clinical actions on timelines shorter than those for drug and vaccine development. Here, we focus on zinc deficiency symptoms, symptom overlap with other conditions, as well as zinc effects on immune health and mechanistic zinc deficiency risk groups. There are well-studied beneficial effects of zinc on the immune system including a decreased susceptibility to and improved clinical outcomes for infectious pathogens including multiple viruses. Zinc is also an anti-inflammatory and anti-oxidative stress agent, relevant to some severe Coronavirus Disease 2019 (COVID-19) symptoms. Unfortunately, zinc deficiency is common worldwide and not exclusive to the developing world. Lifestyle choices and preexisting conditions alone can result in zinc deficiency, and we compile zinc risk groups based on a review of the literature. It is also important to distinguish chronic zinc deficiency from deficiency acquired upon viral infection and immune response and their different supplementation strategies. Zinc is being considered as prophylactic or adjunct therapy for COVID-19, with 12 clinical trials underway, highlighting the relevance of this trace element for global pandemics. Using the example of zinc, we show that there is a critical need for a deeper understanding of essential trace elements in human health, and the resulting deficiency symptoms and their overlap with other conditions. This knowledge will directly support human immune health for decreasing susceptibility, shortening illness duration, and preventing progression to severe cases in the current and future pandemics.  相似文献   

19.
20.
Impaired immune function in dietary zinc (Zn) deficiency is characterized in part by reduced lymphocyte numbers (lymphopenia) and depressed cell-mediated (T lymphocyte) immune function, however, the causative mechanisms at the molecular level have not been elucidated. This paper will focus on the role of dietary Zn in T lymphocyte signal transduction, and specifically, the early Zn-dependent steps for phosphorylation and the putative Zn-finger proteins or Zn-metalloenzymes that may be part of the molecular mechanism for explaining immune dysfunction in Zn deficiency. One of the major recent findings is that murine splenic T lymphocyte p56lck expression is elevated in dietary Zn deficiency and caloric deficiency. Based on the known functions of p56lck, it is proposed that elevated p56lck may contribute to altered thymocyte maturation, apoptosis, and lymphopenia in dietary Zn deficiency and other malnutrition syndromes.  相似文献   

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