血和尿Ⅳ型胶原对早期糖尿病肾病诊断的意义

目的：探讨血和尿Ⅳ型胶原（ⅣＣ）含量在非胰岛素依赖型糖尿病（ＮＩＤＤＭ）中的变化及对肾功能损害早期诊断的价值。方法：采用酶联免疫法和放射免疫法测定３３例病史５年以上、血尿素氮（ＢＵＮ）和肌酐（ＳＣｒ）均在正常范围内的ＮＩＤＤＭ患者（糖尿病组）和３０例非糖尿病患者（对照组）血和尿中ⅣＣ含量及尿微量白蛋白（ＵＡ）含量,比较２组患者上述各项指标及检测阳性率。结果：糖尿病患者血和尿中ⅣＣ阳性率（分别为７８．７９％和１００．００％）及其含量〔血ⅣＣ（１６０．２０±６６．０１）μｇ／Ｌ,尿ⅣＣ（６７．３５±８．３１）μｇ／Ｌ）〕均明显高于对照组〔分别为１０．００％、６．６７％、（６１．７８±２９．２６）μｇ／Ｌ和（２．２６±２．３６）μｇ／Ｌ〕,Ｐ均＜０．０１。且糖尿病患者尿ⅣＣ检测阳性率（１００．００％）明显高于尿微量白蛋白检测阳性率（１８．１８％,Ｐ＜０．０１）,其含量变化二者呈明显正相关（ｒ＝０．８９２４,Ｐ＜０．０１）。结论：测定糖尿病患者血、尿ⅣＣ,尤其是尿ⅣＣ较尿ＵＡ测定对ＤＮ更具早期诊断价值;ⅣＣ是早期糖尿病肾损害的预警指标之一。     

急性脑出血血浆神经肽Y含量变化及其临床意义

目的：探讨血浆神经肽Ｙ（ＮＰＹ）在急性脑出血中的作用及与血压的相关性。方法：用放射免疫分析法测定４３例急性脑出血患者和正常对照组２５例的血浆ＮＰＹ含量。结果：脑出血组血浆ＮＰＹ含量〔（８３．２２±１７．８７）ｎｇ／Ｌ〕高于正常对照组〔（７１．２４±１１．２３）ｎｇ／Ｌ〕，Ｐ＜０．０１；出血量＞５０ｍｌ者，血浆ＮＰＹ含量〔（９６．６４±１８．６９）ｎｇ／Ｌ〕高于出血量≤５０ｍｌ者〔（７８．７４±１５．３８）ｎｇ／Ｌ〕，Ｐ＜０．０１；随血浆ＮＰＹ含量增高而收缩压逐渐上升；血浆ＮＰＹ含量与收缩压呈正相关（ｒ＝０．８０８，Ｐ＜０．０１），３３例存活者血浆ＮＰＹ含量〔（７９．６８±１５．４９）ｎｇ／Ｌ〕低于１０例死亡者的血浆ＮＰＹ含量〔（９４．９１±２０．９８）ｎｇ／Ｌ〕，Ｐ＜０．０５。结论：脑出血患者血浆ＮＰＹ含量增高与血压呈正相关，故ＮＰＹ增高可作为脑出血患者的危险因素之一。因此，测定脑出血患者早期血浆ＮＰＹ含量对估计伤情和判断预后具有一定的帮助。     

中西医结合治疗慢性肾功能衰竭临床研究

目的：探讨慢性肾功能衰竭有效的非透析治疗方法,以提高治愈率。方法：慢性肾功能衰竭患者１３４例,随机分为治疗组６８例和对照组６６例。对照组采用常规西药治疗;治疗组在西药治疗的基础上加用降氮汤灌肠治疗,其中２６例根据临床辨证分型给予口服中药治疗。２组均以２０日为１个疗程。结果：治疗组治疗后血尿素氮〔ＢＵＮ,（１７．４６±６．８７）ｍｍｏｌ／Ｌ〕和血肌酐〔ＳＣｒ,（６３８．００±２１０．２０）μｍｏｌ／Ｌ〕均显著低于对照组〔分别为（２０．８０±６．４０）ｍｍｏｌ／Ｌ和（８１０．００±２１２．２０）μｍｏｌ／Ｌ〕,Ｐ均＜０．０５;血浆总蛋白和白蛋白〔分别为（５９．２０±２．８０）ｇ／Ｌ和（３７．２０±２．１０）ｇ／Ｌ〕均显著高于对照组〔分别为（５３．４０±２．６０）ｇ／Ｌ和（３０．２０±２．１０）ｇ／Ｌ〕,Ｐ均＜０．０５。治疗组总有效率为８５．３０％,对照组为６５．２０％,２组疗效差异显著（Ｐ＜０．０５）。结论：中西医结合治疗慢性肾功能衰竭可降低血ＢＵＮ、ＳＣｒ,升高血浆总蛋白和白蛋白,改善肾功能,疗效优于单纯西医药治疗。     

新生儿休克时血浆肿瘤坏死因子的测定及其意义

目的：探讨肿瘤坏死因子（ＴＮＦ）在新生儿休克中的作用。方法：应用放射免疫方法检测３６例新生儿休克患儿血浆ＴＮＦ水平。结果：休克组治疗前血浆ＴＮＦ浓度〔（６０４．２６±１．２６）ｎｇ／Ｌ〕显著高于正常对照组〔（３２８．３８±１．１５）ｎｇ／Ｌ〕，Ｐ＜０．０１；感染性休克组〔（６５６．１４±１．４６）ｎｇ／Ｌ〕高于非感染性休克组〔（４６８．７９±１．３２）ｎｇ／Ｌ〕，Ｐ＜０．０５；死亡组〔（６８６．１３±１．１９）ｎｇ／Ｌ〕高于存活组〔（４７１．２３±１．２９）ｎｇ／Ｌ〕，Ｐ＜０．０５。血浆ＴＮＦ浓度与患儿器官损伤数呈正相关趋势，ｒ＝０．３１，Ｐ＞０．０５。结论：ＴＮＦ参与新生儿休克的病理生理过程，且与休克预后有关     

血清酮体比值判断感染性多脏器功能失常综合征病情严重程度及预后的意义

目的：探讨血清酮体比值（ＡＫＢＲ）对判断感染性多脏器功能失常综合征病情轻重程度和预后的意义。方法：测定正常对照组、肝硬化组、急性感染组（又分Ａ、Ｂ、Ｃ３组）患者乙酰乙酸（ＡｃＡｃ）、β羟丁酸（３ＨＢ）及ＡＫＢＲ等指标水平。结果：肝硬化组ＡｃＡｃ〔（０．４２±０．１５）ｍｍｏｌ／Ｌ〕和３ＨＢ〔（０．８２±０．１８）ｍｍｏｌ／Ｌ〕明显低于正常对照组〔（０．９９±０．２０）ｍｍｏｌ／Ｌ和（１．４０±０．２５）ｍｍｏｌ／Ｌ〕，Ｐ均＜０．０１；急性感染Ａ、Ｂ、Ｃ３组的ＰａＯ２、乳酸、阴离子间隙具有显著性差异（Ｐ均＜０．０１）；ＡＫＢＲ与ＡＰＡＣＨＥⅢ评分呈明显负相关（ｒ＝－０．８１２，Ｐ＜０．００１）；血清酮体水平与ＡＰＡＣＨＥⅢ评分间无明显直线相关关系（ｒ＝０．１６３，Ｐ＞０．０５）；ＡＫＢＲ和ＰａＯ２与ＡＰＡＣＨＥⅢ评分间有明显相关性（ｒ＝０．７２２，Ｐ＜０．０１）。结论：ＡＫＢＲ能更早期、直接、准确地反映肝细胞线粒体的受损程度和能量代谢状态，可以作为评估感染性ＭＯＤＳ病情严重程度及预后的重要指标。     

血清可溶性白细胞介素-2受体水平在预测高血压急性脑出血手术治疗中的意义

目的：探讨血清可溶性白细胞介素２受体（ＳＩＬ２Ｒ）水平在预测高血压急性脑出血（ＨＡＣＨ）患者手术治疗中的意义。方法：采用双抗体夹心酶联免疫吸附法测定２０例正常人及４９例ＨＡＣＨ急性期手术和非手术患者血清ＳＩＬ２Ｒ含量。结果：ＨＡＣＨ患者入院当日血清中ＳＩＬ２Ｒ含量〔（０．５９２±０．０３７）Ｕ／Ｌ〕显著高于正常对照组〔（０．２３７±０．０６９）Ｕ／Ｌ〕；手术组患者术前与术后第１天和第１０天血清ＳＩＬ２Ｒ含量比较分别为无显著性差异（Ｐ＞０．０５）和有显著性差异（Ｐ＜０．０１）；手术组患者术后第１日和第１０日与非手术组患者血清ＳＩＬ２Ｒ含量同步比较分别为无显著性差异（Ｐ＞０．０５）和有显著性差异（Ｐ＜０．０５）；死亡患者入院当日血清ＳＩＬ２Ｒ含量〔（０．７４３±０．０４９）Ｕ／Ｌ〕高于存活组〔（０．５９８±０．０４４）Ｕ／Ｌ，Ｐ＜０．０１〕，且显著高于对照组〔０．２３７±０．０６８）Ｕ／Ｌ，Ｐ＜０．０１〕。结论：ＳＩＬ２Ｒ与ＨＡＣＨ患者免疫功能紊乱有关，动态测定血清ＳＩＬ２Ｒ含量，可作为观察ＨＡＣＨ病情发展变化的一项指标，同时对判断ＨＡＣＨ的预后亦有一定临床意义。     

肝硬化合并上消化道出血患者血清胃泌素检测及其临床意义

目的：研究肝硬化合并各种上消化道出血患者血清胃泌素水平变化的临床意义。方法：肝硬化合并上消化道出血患者４６例,无肝硬化上消化道出血患者３１例,均行内镜检查明确诊断,并与正常对照组４０例一起采用放射免疫分析法测定空腹血清胃泌素水平。结果：肝硬化合并食管静脉曲张破裂出血、门静脉高压性胃病出血及无肝硬化胃溃疡患者血清胃泌素〔分别为（７４．５９±２９．２６）ｎｇ／Ｌ、（７６．５２±２０．３４）ｎｇ／Ｌ和（９８．４０±１８．３０）ｎｇ／Ｌ〕与正常对照组〔（６４．４２±２３．２０）ｎｇ／Ｌ〕比较均无显著性差异（Ｐ均＞０．０５）。肝硬化合并胃、十二指肠溃疡及无肝硬化合并糜烂出血性胃炎和十二指肠溃疡患者血清胃泌素〔分别为（１０７．３１±１８．０２）ｎｇ／Ｌ、（１２８．３５±２６．８６）ｎｇ／Ｌ、（１３３．０４±２２．４３）ｎｇ／Ｌ和（１１６．４１±２８．２５）ｎｇ／Ｌ〕与正常对照组比较均有显著性差异（Ｐ＜０．０５或Ｐ＜０．０１）。ＨＰ阳性者血清胃泌素〔（１４２．０１±２７．８６）ｎｇ／Ｌ〕显著高于ＨＰ阴性者〔（７７．２８±２５．１１）ｎｇ／Ｌ,Ｐ＜０．０１〕。结论：血清胃泌素检测有利于肝硬化合并上消化道出血的鉴别诊断     

脑出血患者血浆血小板α—颗粒膜蛋白的变化及其临床意义

目的：探讨脑出血患者血浆血小板α颗粒膜蛋白（ＧＭＰ１４０）含量的变化和临床意义。方法：用放射免疫分析法测定９０例脑出血患者和７０例正常人血浆ＧＭＰ１４０的含量。结果：脑出血患者血浆ＧＭＰ１４０含量于发病１周内达高峰〔（２６．５４±７．２１）μｇ／Ｌ〕，明显高于正常对照组〔（９．０２±２．８９）μｇ／Ｌ，Ｐ＜０．０１〕，以后逐渐下降，第３周末多数降为正常〔（９．６５±３．４０）μｇ／Ｌ〕。出血量＞５０ｍｌ组血浆ＧＭＰ１４０含量〔（３９．５８±７．２９）μｇ／Ｌ〕显著高于出血量＜２０ｍｌ组〔（１５．３５±３．９０）μｇ／Ｌ，Ｐ＜０．０１〕；重型组血浆ＧＭＰ１４０含量〔（３２．１８±６．８１）μｇ／Ｌ〕明显高于轻型组〔（１３．０２±３．２１）μｇ／Ｌ，Ｐ＜０．０１〕；恶化死亡组血浆ＧＭＰ１４０含量〔（３３．３１±８．４５）μｇ／Ｌ〕明显高于治愈组〔（１４．６５±５．３４）μｇ／Ｌ，Ｐ＜０．０１〕。结论：测定脑出血患者血浆ＧＭＰ１４０含量可作为临床上估计出血量、监测病情和判断预后的一个指标。     

血小板活化因子拮抗剂对急性出血坏死型胰腺炎大鼠内毒素血症的防治作用

目的：观察血小板活化因子（ＰＡＦ）拮抗剂对急性出血坏死型胰腺炎（ＡＨＮＰ）大鼠内毒素血症的防治作用。方法：１４０只ＳＤ大鼠随机分为３组：急性胰腺炎组（ＡＰ组）：采用去氧胆酸钠逆行胰管内注射法复制；治疗组（ＢＮ组）：制备模型后经腹腔注射ＰＡＦ特异性受体拮抗剂ＢＮ５２０２１（５ｍｇ／ｋｇ）；假手术组（ＳＯ组）：开腹后仅轻轻翻动胰腺即关腹。结果：ＢＮ组与ＡＰ组比较，１小时后血清淀粉酶值明显下降〔（１４９７０±２５００）Ｕ／Ｌ，（１６１７０±２３８０）Ｕ／Ｌ，Ｐ＜０．０５〕，６小时和１２小时后更为明显（Ｐ均＜０．０１）；血中ＰＡＦ含量１小时后明显降低〔（２．２０±０．２５）μｇ／Ｌ与（１．１０±０．２１）μｇ／Ｌ，Ｐ＜０．０５〕，３小时后更为明显（Ｐ＜０．０１）。血浆内毒素含量ＢＮ组比ＡＰ组明显下降（Ｐ＜０．０１）。ＢＮ组术后大鼠平均存活时间为（４５．０±２５．１）小时，存活率为４０％；ＡＰ组术后大鼠在２４小时内全部死亡，平均存活时间为（１１．５±４．８）小时，存活率为０（Ｐ均＜０．０１）。结论：ＰＡＦ参与了ＡＨＮＰ的发病过程；应用ＰＡＦ受体拮抗剂对实验性ＡＨＮＰ有良好的防治作用。     

内源性洋地黄因子与原发性高血压胰岛素抵抗

目的：探讨内源性洋地黄因子（ＥＤＬＦ）在胰岛素抵抗（ＩＲ）的原发性高血压（ＥＨ）发病中的作用。方法：对３０例ＥＨ患者（ＥＨ组）行葡萄糖耐量及胰岛素释放试验，测定其血清ＥＤＬＦ，并与１６例正常血压者（ＮＴ组）作对照。结果：ＥＨ组患者血清ＥＤＬＦ〔（１５４．４０±４６．８７）ｎｇ／Ｌ〕显著高于ＮＴ组〔（１２２．２９±２４．０６）ｎｇ／Ｌ，Ｐ＜０．０１〕；ＥＨ组空腹血浆胰岛素与体重、体重指数（ＢＭＩ）、臀围及ＥＤＬＦ呈显著正相关（ｒ值依次为０．５２，０．３５，０．４５和０．４１，Ｐ＜０．００２５、Ｐ＜０．０５、Ｐ＜０．０１和Ｐ＜０．０２５）。结论：ＥＨ患者存在明显的ＩＲ和血清ＥＤＬＦ升高，并由此引起持续的高血压     

Sodium balance and osmolarity in burn patients

In 12 severely burned patients the input of fluid and sodium, as well as sodium concentration in plasma and urine, was studied. The osmolarity in plasma and 24-h urine was measured. The high initial sodium input is noted. Plasma sodium levels stay within the normal range when the amount of sodium given during the further treatment is reduced. The importance of urea production in affecting plasma osmolarity is demonstrated.     

Methanol poisoning

Methanol poisoning is an uncommon but an extremely hazardous intoxication. Since methanol is a versatile fuel and is having increasing usage in an energy-conscious society, a high index of suspicion and swift laboratory confirmation is essential in managing this poisoning. Methanol poisoning may occur in sporadic or epidemic circumstances. Chronic exposure may occur in the occupational setting. Man is uniquely susceptible to methanol toxicity, perhaps dependent upon folate metabolism. Classic symptoms of methanol toxicity can only occur in laboratory animals who are rendered folate deficient. Folate may be useful in humans enhancing removal of the toxic products of methanol poisoning. The enzyme responsible for metabolism of methanol is alcohol dehydrogenase. Ethanol has a higher affinity for this enzyme and is preferentially metabolized. Simultaneous ethanol and methanol administration may confuse the onset of the intoxication. Pyrazoles may also be used to inhibit alcohol dehydrogenase thus preventing the intoxication. The most important initial symptom of methanol poisoning is visual disturbance. The symptoms may be delayed up to 24 hours after ingestion due to simultaneous alcohol administration and metabolic processes. Laboratory evidence of severe metabolic acidosis with increased anion and osmolar gaps strongly suggest the clinical diagnosis. There may be an important association between mean corpuscular volume which is significantly higher in cases of severe methanol poisoning than in mild cases.(ABSTRACT TRUNCATED AT 250 WORDS)     

A multidisciplinary consensus on dehydration: definitions,diagnostic methods and clinical implications

Background: Dehydration appears prevalent, costly and associated with adverse outcomes. We sought to generate consensus on such key issues and elucidate need for further scientific enquiry.

Materials and methods: A modified Delphi process combined expert opinion and evidence appraisal. Twelve relevant experts addressed dehydration’s definition, objective markers and impact on physiology and outcome.

Results: Fifteen consensus statements and seven research recommendations were generated. Key findings, evidenced in detail, were that there is no universally accepted definition for dehydration; hydration assessment is complex and requires combining physiological and laboratory variables; “dehydration” and “hypovolaemia” are incorrectly used interchangeably; abnormal hydration status includes relative and/or absolute abnormalities in body water and serum/plasma osmolality (pOsm); raised pOsm usually indicates dehydration; direct measurement of pOsm is the gold standard for determining dehydration; pOsm >300 and ≤280 mOsm/kg classifies a person as hyper or hypo-osmolar; outside extremes, signs of adult dehydration are subtle and unreliable; dehydration is common in hospitals and care homes and associated with poorer outcomes.

Discussion: Dehydration poses risk to public health. Dehydration is under-recognized and poorly managed in hospital and community-based care. Further research is required to improve assessment and management of dehydration and the authors have made recommendations to focus academic endeavours.

• Key messages

• Dehydration assessment is a major clinical challenge due to a complex, varying pathophysiology, non-specific clinical presentations and the lack of international consensus on definition and diagnosis.

• Plasma osmolality represents a valuable, objective surrogate marker of hypertonic dehydration which is underutilized in clinical practice.

• Dehydration is prevalent within the healthcare setting and in the community, and appears associated with increased morbidity and mortality.

     

Global end-diastolic volume, serum osmolarity, and albumin are risk factors for increased extravascular lung water

Background

The transpulmonary thermodilution technique allows the determination of cardiac preload (global end-diastolic volume index) and quantification of pulmonary edema (extravascular lung water index [EVLWI]). Pulmonary edema commonly develops in critically ill patients; however, the underlying pathophysiology, that is, hydrostatic (cardiac) or permeability-induced (noncardiac), often remains unclear. In this study, hemodynamic and serum parameters of osmolarity and oncotic pressure were analyzed to identify risk factors for increased EVLWI.

Methods

A retrospective, single-center analysis in an intensive care unit of a university hospital was performed. No interventions were made for the study. Forty-two critically ill patients were included, and 126 simultaneous hemodynamic measurements and serum determinations were analyzed by logistic regression and Spearman rank correlation coefficient analysis.

Results

Global end-diastolic volume index (P = .001), serum albumin (P = .006), and serum osmolarity (P = .029) were significant factors for increased EVLWI (defined as >10 mL/kg).

Conclusion

Hypervolemia, hypoalbuminemia, and high plasma osmolarity are associated with increased EVLWI.     

Muscular venous blood metabolites during rhythmic forearm exercise while breathing air or normoxic helium and argon gas mixtures

Summary. The effects of breathing normoxic helium or argon gas mixture on the local muscular metabolism during exercise were compared to those of room air in four healthy subjects. For this purpose, Po₂, Pco₂, pH, the concentrations of lactate (LA), glucose (Gl) haemoglobin (Hb) and K⁺ and osmolarity were repeatedly measured in efferent muscular venous blood during 12 min of rhythmic forearm exercise and 16 min of recovery. The time courses and magnitude of the changes in Pco₂, pH, [Gl], [Hb], [K⁺] and osmolarity during exercise and recovery were similar for breathing both the helium and argon gas mixtures. The main finding was that during exercise, the [LA] curve reached a peak value significantly higher by 25% under normoxic helium than under room air or normoxic argon breathing. This rise in [LA] was accompanied by a slight reduction in muscular venous Po₂, too small to signify muscular hypoxia. The possibility that this decline in Po₂ might be due to a shift in muscular metabolism towards lipid oxidation was confirmed by the lower muscular respiratory quotient observed during helium breathing. However, such a shift did not explain why [LA] rose during this breathing. The probable explanation is that helium facilitates LA diffusion out of the myocytes.     

Migraine and genetic and acquired vasculopathies

It is remarkable that migraine is a prominent part of the phenotype of several genetic vasculopathies, including cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL), retinal vasculopathy with cerebral leukodystrophy (RVCL) and hereditary infantile hemiparessis, retinal arteriolar tortuosity and leukoencephalopahty (HIHRATL). The mechanisms by which these genetic vasculopathies give rise to migraine are still unclear. Common genetic susceptibility, increased susceptibility to cortical spreading depression (CSD) and vascular endothelial dysfunction are among the possible explanations. The relation between migraine and acquired vasculopathies such as ischaemic stroke and coronary heart disease has long been established, further supporting a role of the (cerebral) blood vessels in migraine. This review focuses on genetic and acquired vasculopathies associated with migraine. We speculate how genetic and acquired vascular mechanisms might be involved in migraine.     

Fibrinogen and fibrin structure and functions

Fibrinogen molecules are comprised of two sets of disulfide-bridged Aalpha-, Bbeta-, and gamma-chains. Each molecule contains two outer D domains connected to a central E domain by a coiled-coil segment. Fibrin is formed after thrombin cleavage of fibrinopeptide A (FPA) from fibrinogen Aalpha-chains, thus initiating fibrin polymerization. Double-stranded fibrils form through end-to-middle domain (D:E) associations, and concomitant lateral fibril associations and branching create a clot network. Fibrin assembly facilitates intermolecular antiparallel C-terminal alignment of gamma-chain pairs, which are then covalently 'cross-linked' by factor XIII ('plasma protransglutaminase') or XIIIa to form 'gamma-dimers'. In addition to its primary role of providing scaffolding for the intravascular thrombus and also accounting for important clot viscoelastic properties, fibrin(ogen) participates in other biologic functions involving unique binding sites, some of which become exposed as a consequence of fibrin formation. This review provides details about fibrinogen and fibrin structure, and correlates this information with biological functions that include: (i) suppression of plasma factor XIII-mediated cross-linking activity in blood by binding the factor XIII A2B2 complex. (ii) Non-substrate thrombin binding to fibrin, termed antithrombin I (AT-I), which down-regulates thrombin generation in clotting blood. (iii) Tissue-type plasminogen activator (tPA)-stimulated plasminogen activation by fibrin that results from formation of a ternary tPA-plasminogen-fibrin complex. Binding of inhibitors such as alpha2-antiplasmin, plasminogen activator inhibitor-2, lipoprotein(a), or histidine-rich glycoprotein, impairs plasminogen activation. (iv) Enhanced interactions with the extracellular matrix by binding of fibronectin to fibrin(ogen). (v) Molecular and cellular interactions of fibrin beta15-42. This sequence binds to heparin and mediates platelet and endothelial cell spreading, fibroblast proliferation, and capillary tube formation. Interactions between beta15-42 and vascular endothelial (VE)-cadherin, an endothelial cell receptor, also promote capillary tube formation and angiogenesis. These activities are enhanced by binding of growth factors like fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor (VEGF), and cytokines like interleukin (IL)-1. (vi) Fibrinogen binding to the platelet alpha(IIb)beta3 receptor, which is important for incorporating platelets into a developing thrombus. (vii) Leukocyte binding to fibrin(ogen) via integrin alpha(M)beta2 (Mac-1), which is a high affinity receptor on stimulated monocytes and neutrophils.     

Telemedicine and teleradiology technologies and applications

Summary. Telemedicine and teleradiology hold the key for improving future health care delivery. In this paper we first review current communication and computer technologies used in telemedicine and teleradiology. Five examples in teleradiology applications are given including hospital-integrated picture archiving and communication systems, tele-neuro-imaging, telemammography, university consortium teleradiology service, and teleradiology for second opinion. Parameters important to teleradiology applications like costs, image quality, system reliability, and turn around time are considered. Data security is discussed, including patient confidentiality and image authenticity-which will be a major issue in future teleradiology applications.