不同年龄组儿童甲状腺测量值及其变化的研究

调查了90具童尸用状腺的基本形态,可分四型。其中以甲状腺由两侧叶及峡部组成者为最多,占50.22%。测量了甲状腺各部的长、宽、厚。分年龄组进行了数据的统计学处理,并计算出儿童与成人甲状腺各部相应值的百分比。结果显示:小儿甲状腺侧叶的长度和宽度在幼儿期(1—3岁)就已发育近成人的一半。随着年龄的增长,甲状腺各部的均值逐渐增加。除各部的宽度以及锥体叶的长度外,各相邻两组间同项均数的比较,经双侧T检验发现差异具有高度显著性(P<0.01)。     

Hemodynamics in congenital heart disease

This paper introduces a very general and flexible model for the study of hemodynamic changes in congenital heart disease. The generality of the model makes it possible to use the same computer program (which is included in an Appendix) to study both the fetal circulation and the adult circulation, as well as such diverse disease states as patent ductus arteriosus, ventricular septal defect, atrial septal defect, tetralogy of Fallot and transposition of the great arteries. In this paper, only patent ductus and ventricular or atrial septal defect are studied, with special emphasis on the influence of increasing pulmonary vascular resistance on the shunt flow. In the case of patent ductus and ventricular septal defect, the computed shunt flow is very time-dependent and the left-to-right shunt becomes first bidirectional and then right-to-left as the pulmonary resistance increases. By contrast, the computed shunt flow of atrial septal defect is nearly time-independent and is also somewhat less sensitive to the pulmonary vascular resistance.     

钙拮抗剂对出血性休克犬重要器官组织中黄嘌呤氧化酶活性的影响

在休克过程中，体内活性氧代谢与细胞内钙超负荷存在着相互影响。为了研究林克和复苏过程中钙拮抗剂对脂质过氧化的影响，用１７只杂种犬快速放血使平均动脉压为５．３２ｋｐｄ，并维持９０ｍｉｎ。然后回输全部失血。在休克３０ｍｉｎ时，各组别静脉注射（１５ｍｉｎ内）硫氮酮（４０ｇ／ｋｇ·ｍｉｎ￣（－１）），异搏定（１０μｇ／ｋｇ·ｍｉｎ￣（－１）），或等量生理盐水。复苏后１５０ｍｉｎ处死动物，取心、肝、肺、肾、胰和小肠组织备检。结果显示，用硫氮酮和异搏定治疗组，各主要脏器组织中黄嘌呤氧化酶活性和丙二醛含量均显著低于休克对照组。而各检测组织中超氧化物歧化酶活性变化不一。这些资料显示钙拮抗剂抗休克的机制与其阻滞Ｃａ２＋内流，降低组织中黄嘌呤氧化酶活性，抑制脂质过氧化有密切关系。     

Laryngeal and velopharyngeal sensory impairment in obstructive sleep apnea

STUDY OBJECTIVE: To determine whether mucosal sensory dysfunction is present at multiple upper-airway sites in patients with obstructive sleep apnea (OSA). DESIGN: Physiologic testing of consecutive patients with OSA and nonsnoring controls. SETTING: University hospital sleep center. PARTICIPANTS: Thirty-nine subjects with OSA and 17 controls. INTERVENTIONS: Endoscopic testing was used to determine sensory detection thresholds for air-pressure pulses delivered to the oropharynx, velopharynx, hypopharynx, and larynx (aryepiglottic eminence). The air-pulse stimulus intensity required to elicit the protective laryngeal adductor reflex was also determined. MEASUREMENTS AND RESULTS: There was a significant impairment in sensory detection threshold for OSA versus control subjects in the oropharynx, as previously described by ourselves using other techniques, as well as at the velopharynx (median 11 mm Hg [confidence interval 9-11] for subjects with OSA vs 8 mm Hg [confidence interval 4-11] for controls, P = .03) and, at the larynx, 4 mm Hg [confidence interval 2-9] for subjects with OSA vs 2 mm Hg [confidence interval 2-3] for controls, P < .001). The threshold stimulus intensity for the laryngeal adductor reflex was also significantly higher for OSA subjects. For OSA patients with abnormal laryngeal sensation (61% of OSA subjects), there were significant correlations between laryngeal sensory values and measures of apnea severity, including apnea-hypopnea index (r = 0.82, P < .001) and nadir SaO2 (r = -0.48, P < .05). CONCLUSION: Mucosal sensory function is impaired at multiple upper-airway sites in OSA.     

低频超声透皮给药的研究进展与应用

低频超声可以增强包括大分子药物在内的许多药物的透皮传输,其主要机制是超声的空化作用,大多数人认为是通过改变角质层角化细胞排列结构来提高皮肤渗透能力的.低频超声透皮给药已被人们用于离体实验和动物活体实验,到目前为止,无论是小分子透皮传输还是大分子透皮传输都有很多成功的例子.但是真正通过低频超声透皮导入药物进行治疗的临床应用报道很少,需要更进一步大量的临床试验以确定其安全性与实用价值.一旦其安全性得以证实,合适的低频超声透皮仪研制成功,低频超声快速透皮必将成为一种安全、有效、可控、经济的新型给药方式.     

Novel method for the quantitative assessment of cell migration: a study on the motility of rabbit anterior cruciate (ACL) and medial collateral ligament (MCL) cells

A novel method of quantitating cell migration has been proposed for the potential utilization of tissue engineered scaffolds. Applying Alt's conservation law to describe the motion of first passage ACL and MCL cells, we have developed a quantitative method to assess innate differences in the motility of cells from these two ligamentous tissues. In this study, first passage ACL and MCL cells were cultured from four mature New Zealand white rabbits. One side of the cell monolayer was scraped completely away to create a wound model. The cell moved into the cell-free area, and cell density profiles were analyzed at 6 h and 12 h. Values of the random motility coefficient (mu) were then estimated by curve fitting the 6 h and 12 h data to a mathematical model, derived from the conservation law of cell flux. During 6 h of incubation in medium supplemented with 1% FBS, MCL cells (mu(MCL) = 4.63 +/- 0.65 X 10(-6) mm(2)/sec) were significantly (p < 0.05) more mobile than ACL cells (mu(ACL) = 2.51 +/- 0.31 X 10(-6) mm(2)/sec). At 12 h, the MCL cells also appeared to move faster (mu(ACL) = 4.39 +/- 0.63 X 10(-6) mm(2)/sec, mu(MCL) = 6.59 +/- 1.47 X 10(-6) mm(2)/sec), but the difference was not statistically significant (p = 0.18). Exposure of the cells to growth factors PDGF-BB or bFGF for 6 h had no significant effect on the migration of the ACL and MCL cells. However, exposure of the ACL cells (p < 0.05) and the MCL cells (p = 0.19) to 1 ng/mL of PDGFBB for 12 h enhanced their migration. Incubation with a high concentration (100 ng/mL) of PDGF-BB or bFGF at concentrations tested (1 or 100 ng/mL) for 12 h, produced little or no migratory stimulation on these ligament cells. Our findings support the previous qualitative observations made by numerous investigators. The novel methodology developed in this study may provide a basis for tissue engineering, and the results may be applied to tissue reconstruction techniques of the knee ligaments.     

Human hepatic lipase mutations and polymorphisms.

Human hepatic lipase (HL) is a 477 residue glycoprotein that hydrolyzes triglycerides from plasma lipoproteins. Familial HL deficiency is a rare recessive disorder that is characterized by premature atherosclerosis and abnormal circulating lipoproteins. While studying the HL gene from the world's index family with HL deficiency, we identified four coding sequence variants of HL, one in each of exons 4, 5, 6, and 8. In this report we present the genetic basis for two new HL gene variants, one in each of exons 3 and 5. All six HL DNA variants are single base pair changes. Two variants (at codons 133 and 202) are diallelic DNA polymorphisms that are silent at the amino acid level. One variant (V73M) is an allele that defines an uncommon HL isoprotein. One variant (N193S) has two alleles of approximately equal frequency in the population that specify two common HL isoproteins. Two variants (S267F and T383M) are rare mutations found to date only in HL deficient subjects and their relatives. Of the six HL variants described to date, only S267F and T383M are associated with hyperlipidemia.     

Cloning and developmental expression analysis of the murine homolog of the spinocerebellar ataxia type 1 gene (Sca1)

Spinocerebellar ataxia type 1 (SCA1) is an autosomal dominant neurodegenerative disorder caused by the expansion of a CAG trinucleotide repeat which encodes glutamine in the novel protein ataxin-1. In order to characterize the developmental expression pattern of SCA1 and to identify putative functional domains in ataxin-1, the murine homolog (Sca1) was isolated. Cloning and characterization of the murine Sca1 gene revealed that the gene organization is similar to that of the human gene. The murine and human ataxin-1 are highly homologous but the CAG repeat is virtually absent in the mouse sequence suggesting that the polyglutamine stretch is not essential for the normal function of ataxin-1 in mice. Cellular and developmental expression of the murine homolog was examined using RNA in situ hybridization. During cerebellar development, there is a transient burst of Sca1 expression at postnatal day 14 when the murine cerebellar cortex becomes physiologically functional. There is also marked expression of Sca1 in mesenchymal cells of the intervertebral discs during development of the spinal column. These results suggest that the normal Sca1 gene, has a role at specific stages of both cerebellar and vertebral column development.      

腕关节关节囊内韧带的解剖观察及其创伤学意义

本文描绘了腕关节关节囊内韧带的解剖,其中首次描述了中腕关节的韧带连结,即大、小多角骨,头状骨至舟状骨的韧带和钩骨至三角骨的韧带.本文还论述了与这些韧带连结方式密切相关的腕骨生理运动特点及维持腕关节稳定性的因素.文章还讨论了与腕关节关节囊内韧带有关的腕部创伤学特点.