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In neonates, herpes simplex virus (HSV) infections can lead to severe diseases associated with high mortality. We report a 6-day-old girl who developed clinical signs of fulminant hepatic failure accompanied by infectious-toxic shock and disseminated coagulopathy secondary to HSV type 1 (HSV-1) infection. The diagnosis was performed postmortem by demonstration of HSV-1 DNA in liver tissue as well as by retrospective detection of HSV-specific antibodies.

Because of their localization and function as phagocytes, alveolar macrophages could take part in the catabolism of surfactant, including surfactants used for treatment. Conditions of the ingestion of the surfactant preparation AWD 56-02 by alveolar macrophages in vitro are described in this paper. The surfactant was labeled with rhodaminyl phosphatidylethanolamine and incubated with alveolar macrophages lavaged from rat lungs. Membrane binding and phagocytosis were evaluated by fluorescence microscopy and quantified fluorimetrically after extraction of the dye. The surfactant was phagocytosed only in the presence of rat serum. The opsonins in the serum are related to complement and Fc receptors as demonstrated by the heat lability of the factor and the inhibition by aggregated gamma-globulins. Furthermore, the phagocytosis depends on calcium and on a factor in the surfactant preparation. Experiments with inhibitors and competition with unlabeled surfactant show that the phagocytosis is a specific and energy-dependent process. Catabolism by alveolar macrophages might be an important step in the metabolism of surfactant, especially when administered in pathological conditions characterized by the presence of serum in the airspaces.

The case of a 57-year-old man is reported, who worked as a plasma welder about 15 years. Chronic recurrent bronchitis was diagnosed 12 years after beginning of this work. The patient changed the place of his employment but the course of disease was uncommonly progressive. He died of right ventricular heart failure 10 years later. One year before death, the chronic obstructive pulmonary lesions were acknowledged as occupational disease. The post-mortem histological and chemical analysis of lung tissue yielded a mixed dust pneumoconiosis. These findings supported additionally the diagnosis of occupational disease.

The influence of chronic administration of ambroxol on the phospholipid-(PL-) content and ultrastructure of lungs has been studied and compared with the effect of chlorphentermine (chlph.). Both drugs are amphiphilic substances. The causative factor of the well-known chlph. induced phospholipidosis-like alterations was suggested to be an inhibition of enzymatic degradation of PL. Rats were intraperitoneally treated five times per week for two weeks with chlph. (0,2 mMol per kg b.w.) and ambroxol (0.2 mMol per kg b.w.), respectively. Lung, heart, liver, kidney and spleen were light microscopically examined, and the lung was studied by electron microscopy. Furthermore, the PL-content of the whole lung tissue, the proportion of phosphatidylcholine (PC), the lung weight/body weight ratio (LM/KM) as well as the dry weight/wet weight ratio (TM/FM) of the lung was calculated. The application of chlph, induced an excessive PL-storage in the lung as indicated by an increase of the PL-content, of the PC-proportion as well as of the LM/KM and TM/FM ratio. The accumulated PL are detectable by electron microscopy, mainly in the lysosomes of macrophages appearing as lamellar or crystalloid inclusions. On the contrary, chronic application of ambroxol does not cause any substantial changes especially no abnormal lysosomal PL-inclusions. Therefore, it is suggested that ambroxol does not interfere with the PL-metabolism in a way comparable to that of the chlph. action.

The influence of the amphiphilic drugs imipramine (150 mg/kg b. w./day) and chloroquine (75 mg/kg b. w./day) on the phospholipid (PL) -metabolism of rat lung, its PL-content and PL-composition were measured in the cell free lung lavage fluid (alveolar surfactant), in the free alveolar cells (mainly alveolar macrophages), and in the residual lung tissue. In addition to the long-term administration (15 applications during a period of 3 weeks), the influence of short-term administration (2 or 4 applications, resp., during a period of 2 or 4 days) was examined. The alveolar macrophages show the largest increase in PL-content. As revealed by its composition the stored PL are of surfactant origin. In chloroquine treated rats the number of macrophages is increased as well. The concentration of stored PL is higher in macrophages of imipramine treated rats. The excessive accumulation of PL in this animal group possibly impairs the clearance function of alveolar macrophages. This is suggested to be the reason for the accumulation of alveolar surfactant in imipramine treated rats. The influence of the drugs on the PL-content of the residual lung tissue was weak. The results of this study show that amphiphilic drugs cause an accumulation of surfactant-PL within the alveolar macrophages and can promote the alveolar surfactant content even after short-term application. The role of alveolar macrophages in alveolar surfactant catabolism is demonstrated.

A biopsy taken from the right m. gastrocnemius of a sporadic case of central core disease has been investigated by electronmicroscopy. Both longitudinal and cross sections show cores, which are partially in the centre and partially near the sarcolemma of the muscle fibres. These cores are more or less sharply delimited from the intact areas of the muscle fibres. A zone showing a severe destruction of the regularly fibrillar structure is observed in the centre of each core. This destruction zone is surrounded by a transition zone, in which a partial lesion of the fibrillar structure is found whereas the sarcomeric segmentation is preserved. The width of the interfibrillar sarcoplasm is reduced, frequently, however, mitochondria containing cristae of normal structure are observed. The cores are foundlimited by target fibres. Pathogenetically, the damages of z-lines are assumed to be dominant in the formation of the cores.

A prothrombin complex concentrate produced according to a new procedure was tested for potential thrombogenicity in vitro and in vivo. The results obtained by in vitro methods (NAPTT, TGt50, determination of the hydrolytic index) were not in the critical range of thrombogenicity. An effective dose of 175 U/kg for thrombus formation assessed in the stasis model of Wessler suggested comparatively low thrombogenicity. In the non stasis model no changes in the haemostaseological variables indicative of consumption reaction were observed after infusion of 125 U/kg for 30 min in rabbits. In the organs investigated (heart, liver, kidneys, adrenals) no thrombin were detected morphologically.

Changes in the clotting system, as well as morphological and functional alterations corresponding to that of the pathologic phenomenon of disseminated intravascular coagulation (DIC) or consumption coagulopathy, were produced by thrombin infusion (550 NIH U X kg-1 X h-1) in rats and simultaneous inhibition of fibrinolysis by PAMBA (100 mg/kg). Changes in the fibrinogen level and platelet count as well as the appearances of fibrin monomers and the formation of microthrombi in several organs were evaluated. Simultaneously, the function of the respiratory system was investigated by continuous measurement of oxygen consumption as well as elasticity and water content of the lung. From the time course of the alterations in the several parameters, conclusions can be drawn for the pathogenesis and the possible therapeutic influence on DIC.

The influence of short-term and chronic administration of chlorphentermine (Chlph) on the structure and phospholipid (PL)-content of the lungs was studied in guinea pigs. The drug was given daily in a dose of 40 mg per kg body weight i.p. The PL-content of the whole lung as well as the phosphatidyl choline (PC)-portion were estimated in animals treated with Chlph for 4, 5 and 6 weeks. In a further experiment, the influence of 2, 4 and 28 days application on the PL-content of the lung lavage fluid separated into the acellular and cellular (macrophage) fraction was examined. Morphologic studies of lung, liver, heart, kidney, spleen, brain, and pancreas supplemented the PL-content analysis. The amount of PL in the whole lung increases continuously with the duration of the treatment but only moderately. The PC-fraction of the total PL remains constant throughout the experiment. A substantially greater increase was detected in the lung lavage fluid whereby the cellular fraction is most affected. Very important is the result that the PL-content of the lung lavage fluid reaches its highest level already after two Chlph-injections. After short-term administration the morphological examination of the lung mainly shows inflammatory infiltrations, whereas after long-term application a foam cell reaction is mainly localized in the interstitium. The studies show that an increase of the amount of lung sufactant in guinea pigs is possible following Chlph administration.

After one application of paraquat (35 mg/kg body weight) studies of the changes in lung structure in phospholipid content of the alveolar wash as well as in the static pV-curves are performed on adult hooded rats. Pathomorphologically 2, 4, 8, 16, 24 and 48 h after the paraquat intoxication focal atelectases, circumscribed inflammatory infiltrations of the interstitium are predominant as well as an accumulation of macrophages in the interstitium and in the alveolar space. Initially granulocytes dominate in the inflammatory infiltrates; after 8 h lymphoid elements and histiocytes became more and more apparent. 24 an 48 h after the paraquat injection there is a degradation of the alveolar epithelium. After 8-48 h the phospholipid content of the alveolar wash and after 2-48 h the hysteresis loop of the pV-curves are statistically significantly decreased in comparison with control animals. It is assumed, that the paraquat mediated dearrangement of the surfactant system of the lung is caused by an increased degradation in consequence of liberated phospholipases as well as by a decreased or ceased synthesis of the surfactant. The latter may be the consequence of an autooxydative membrane alteration of the endoplasmatic reticulum, the toxic action of the hydrogen peroxide originated by the autooxydation but also of the loss of energy rich substrates.

Because of recurrent paronychia of the right thumb "granulation" tissue was removed from the nail-bed of a ten-year-old girl. Histological examination revealed a cornified squamous-cell carcinoma. About five months later a lymph-node metastasis was found in the right axilla. After radical dissection of the axillary region further lymph-node metastases were found, as well as a lymphangitic carcinosis with tumour infiltration in the veins. Despite telecobalt radiation there were recurrent retastases which could no longer be removed by operation. Two years after the diagnosis the girl died. Necrospy revealed diffuse tumour infiltration of the soft tissue of the axilla, upper arm, shoulder, neck and thoracic wall on the right, including the breast tissue, with thoracic para-aortic-abdominal and left-sided axillary lymph-node metastases, and lung and pleural metastases bilaterally.

A desmoplastic fibroma of the left humerus with a pathological fracture in a 9-year-old girl is presented. The postoperative course was uncomplicated: no recidive occurred. The histological picture of this rare bone tumor (76 similar cases were reported in the literature) is identical both with aggressive fibromatosis and with the desmoid tumor. It contains areas with abundant collagen fibers and densely packed areas composed of fibrocytes, fibroblasts as well as myofibroblasts. Myofilaments have been detected by electron microscopy in the latter cell type.

Alterations of the lung structure, especially of the pneumocytes type II, of asphyxied newborn rabbits were investigated. Experiments were carried out on pregnant does shocked by thrombin- and Pamba-applications on the 28th, 29th and 30th day of gestation and on their newborns delivered by caesarian section at these days and killed after one or five hours life-time. Histologically, adult rabbits show characteristic alterations in an early phase of the shock. Lung alterations are the main findings in the newborns. Atelectases and, additionally, disturbances of circulation, permeability and also hyaline thrombi are seen. Lamellar bodies within the pneumocytes type II show a significant decrease of the lamellae and the whole osmiophilic material. The alterations of immature newborns are more severe than those of mature animals and also more severe after the longer life-time. These alterations are considered as a result of decreased synthesis of surface active phospholipids.

Intrauterine asphyxia has been induced in immature and mature newborn rabbits by means of experimental shock of the pregnant doe. Typical changes of clotting parameters and morphological alterations in different organs specific for shock were used as criteria of the maternal shock. For the detection of asphyxia conditioned neonatal organ lesions, liver, lung, kidney and heart muscle were studied light microscopically. Special attention was devoted to liver alterations, i.e. changes of hepatocyte structure, glycogen content and microcirculation disturbances as well as to alterations of the hematopoietic system. The asphyxia related effects were vacuolic degeneration of hepatocytes, centroacinar hyperemia and persistence of hematopoietic cells in the neonatal liver. The alterations of the hepatocytes as well as of the hematopoietic system were more conspicuous in mature then in immature asphyxiated rabbits. On the contrary, the microcirculatory changes are similar in both animal groups.

A sporadic case of central core disease in a 5 1/2-year-old girl is reported. Clinically, a retarded motor development existed, furthermore, a muscle weakness and hypotonia of the extremities and trunk, contractures of the hip- and knee-joint,and luxation of both hip-joints. Biopsy specimens are taken from both Mm. gastrocnemii. Muscle fibres show, by morphologic examination, 95 per cent cores, which are characteristic for this myopathy. A further abnormality is seen inthe histochemical preparations for phosphorylase, succinate dehydrogenase, NAD diaphorase tetrazolium reductase, myofibrillar ATPase as well as AS-reaction with and without diastase digestion. With these techniques the muscle fibres show an uniform reaction pattern in which the activities of the oxidative andglycolytic enzymes correspond to the type I fibres of healthy persons. The cores show a lack of a activity of the oxidative and glycolytic enzymes as well as are ATPase- and PAS-negative. By reason of this histochemical behaviour it is suggested that the cores are predominantly unstructured. The cause of this disease might be complex disturbances in the neuro-muscular system manifested in the fetal period.

Alterations of the lung- and lung lavage fluid-phospholipids (PL's) after a maternal thrombin-shock have been studied in 1 and 5 h old newborn rabbits delivered at days 28 and 30 of gestation. In lung wash the amount of PL increases during the period of gestation and during the first hours of life. In asphyxiated mature animals the PL-content is statistically significantly decreased. The very low PL-content of the lung wash in premature born animals is not affected by asphyxia. The amount of phosphatidyl choline (PC) as a percentage of total PL is unchanged in all animals studied. The PL and PC content in the lung tissue follows the same developmental pattern but the differences are not statistically significant. Changes in the lung weight/body weight (LW/BW)--ratio after asphyxia show a disturbed development of the newborn lung, too.

In the course of an experimental poisoning of rats with mercury(II)-chloride no disturbances of haemostasis occurred, from which the development of a consumption coagulopathy might be concluded. Only a diminution of the plasminogen level could be found which is due to a moderate damage of liver parenchyme. The increased activity of the free form of the plasminogen activator found in the kidney homogenate is considered as an enzymatic activation because of kidney cell necrosis.

A report is given on a premature stillborn with severe congenital spinal muscular atrophy, arthrogryposis multiplex congenita and hydrops fetalis. During delivery the head was spontaneously pulled off. The neuromuscular disease was the cause of this unusual complication. No alterations of collagenous fibres were found by light and electron microscopy in dermis, aorta or in the Achilles tendon. The hydrops fetalis was not of immunological nature.

In continuation of previous experiments in adult rats the alteration in content and composition of lung phospholipids (PL) and lung structure of newborn rats of different gestational age was studied after three administrations of the amphiphilic drugs imipramine (75 mg/kg b.w.) and chloroquine (50 mg/kg b.w.). The fetuses were obtained by Cesarean section on day 20, 21, or 22 of gestation. Morphological examinations of the lungs of drug treated 21-day-old fetuses revealed a substantially better aeration than nontreated controls. 20 and 22 days old fetuses showed no differences in aeration between drug and saline treated rats. Analogous results were obtained with respect to the 1 h survival rate of newborns. Furthermore, imipramine and chloroquine cause a premature development of the pneumocytes type II as shown by electron microscopy. An increased PL content as well as disaturated phosphatidylcholine (DSPC) and phosphatidylglycerol (PG) proportion of fetal lungs, especially in animals born on day 21 of gestation, were found after drug treatment. The results suggest an acceleration of maturation of the pneumocytes type II in fetal lungs induced by amphiphilic drugs.

Generalized disseminated intravascular coagulation (DIC) was produced in rats by thrombin infusion (550 NIH U thrombin/kg/h). Changes in the clotting system and morphological alterations were studied with consideration to early lesions. Furthermore, the influence of the antifibrinolytic agent Pamba and the fibrinolytic enzyme ocrase on DIC are studied. Microthrombi and degenerative alterations are increased in parenchymatous organs after thrombin infusion with Pamba is applied, they are decreased when ocrase is given. Alterations are most prominent in the lungs revealing the appearance of a "shock lung". Semiquantitative morphological examinations of lung, liver, kidney and adrenal glands were performed by counting microthrombi. There are marked differences between the test groups.