Several endocrine disorders with increase or deficiency of hormone production may present a skeletal muscle compromise. Those conditions have been considered as metabolic myopathies. Nevertheless, some pathological abnormalities, mainly microvascular changes and the existence of a cell infiltrate, found in endocrine disorders with an autoimmune origin (primary hipothyroidism, hyperthyroidism associated with Graves disease, diabetes mellitus) have permitted classifing them as inflammatory myopathies. Although muscle pathology in diseases with isolated hormone production alteration has been extensively studied, this investigation has not been realized in patients with abnormalities in several endocrine glands. In this work we report the skeletal muscle ultrastructural pathology in a patient with multihormonal disorder.

A 19 years old male patient presented dwarfism with lack of muscular and sexual development. Plasma levels of thyroxin, Cortisol, growth hormone, testosterone, LH and FSH were low . TSH plasma levels were high.

BK polyoma virus is a 40-45 nm DNA virus that was first identified in the urine of an immunosuppressed patient in 1971. BK virus infection often occurs in childhood and is subclinical. The majority of adults have antibodies to the virus. Asymptomatic viruria, ureteral ulceration, and ureteral stenosis have been described with infection in immunosuppressed patients. Renal graft dysfunction and interstitial nephritis have been associated with BK virus. Differentiation between rejection and infection is important. We report a case of a renal transplant patient with BK polyoma virus infection. This case illustrates the variety of methods that can be used for identification of BK polyoma virus.

The patient, a 52 year old female, presented with an asymptomatic rise in serum creatinine (1.4 to 2.1 mg/dl). Her past medical history was significant for a cadaver kidney transplant two years prior for polycystic kidney disease.

Renal function impairment can be found in severe or complicated P. falciparum malaria. Some studies report 2-5% incidence of acute renal failure associated with high mortality (1). Causes of acute renal damage are not clearly understood but massive hemoglobinuria seems unlikely in the majority of cases and different immunopathogenic mechanisms leading to tubulointerstitial nephritis are currently proposed (2). Ultrastructure of renal lesions in malaria have been performed in humans (3) and in some infections of rodents and monkeys (4). These studies report abnormalities mainly in the glomerular area and references to tubular cell pathologic changes are still limited. This work describes tubular and capillary alterations in P. berghei malaria.

P. berghei parasitized erythrocytes (strain from the Swiss Tropical Medicine Institute) were inoculated intraperitoneally in C57BL/6 male mice. Renal samples were obtained at 13th-14th days post-infection when severe illness was evident and parasitaemia reached 40-50%. Samples were processed by routine techniques for transmission electron microscopy and observed in Hitachi H-500 and H-7100 electron microscopes.

It has been shown that cavities or vacuoles are most evident in the posteroventral and antero ventral cochlear nucleus (PVCN & AVCN) of the gerbil. These vacuoles are reported as a neurodegenerative disorder or spongioform degeneration or a dynamic process related to the degree of auditory stimulation or microenvironmental homeostasis in the cochlear nucleus of the gerbil. Little information is avalable on the origin and formation of microcysts in the dorsal cochlear nucleus (DCN) of the gerbil. The aim of this study, was to investigate the possible formation of microcysts in the gerbil DCN after a surgical ligation of the external auditory canal by transmission electron microscopy.

The mongolian gerbil, Meriones unguiculatus,had been acoustically deprived on the right side by a surgical ligation of the external auditory canal at six months old.

Mice expressing the Epstein-Barr virus nuclear antigen-leader protein (EBNA-LP) develop congestive heart failure and atrial thrombosis as early as four months of age. Epstein-Barr virus (EBV) is a common human herpes virus with a complex life cycle involving chronic replication in epithelial tissues. The EBNA-LP, one of six EBV nuclear antigens, has an unknown biochemical function but is associated with EBV-induced growth transformation. This transgenic line was originally produced to investigate oncogenic consequences, but unexpectedly resulted in mice with progressive heart failure. Since the progression and development of the heart failure is highly predictable, this transgenic line may serve as a valuable model for studying the pathophysiologic changes associated with human dilated cardiomyopathy. We describe here the ultrastructural characteristics of the myocardium from EBNA-LP transgenic mice in order to better delineate the pathogenesis of the associated heart disease.

We are participating in a collaborative project at NIOSH on mechanisms of silicosis, in which rats were exposed to filtered air (control) or silica aerosol of 15 mg/m3 (6 hr/day, 5 days/week), with assays conducted at intervals over a 6 month period. We are especially interested in the role of nitric oxide (NO) in the pathophysiology of lung disease. One source of NO is the alveolar macrophage, known to express the inducible form of nitric oxide synthase (iNOS); we used immunohistochemical techniques to determine whether iNOS is upregulated in alveolar macrophages and other lung sources in response to silica.

Silica-exposed and air control animals were sacrificed after 10, 20, 41, 79, and 116 days of exposure. Formalin fixed, paraffin embedded tissues were cut at 5μm, deparaffinized in xylene and rehydrated. Slides were microwaved in citrate buffer, pH 6.0 for antigen retrieval.2 After blocking endogenous peroxidase in 3% H2O2:Methanol (1:1), slides were placed in 10% BSA for 30 min, then incubated overnight in the primary antibody (Monoclonal anti-iNOS, Transduction Laboratories, N32020, 1:50 dilution)

Inhalation injury is present in 32-38% of patients with severe burns and is associated with an increase of 20-84% above the mortality expected based on age and burn size alone. Most previous studies of smoke inhalation injury have utilized large animals such as the sheep and we have previously reported a TEM and SEM study of lung injury in the sheep. The present observations are part of a study to develop a small animal combined model of smoke inhalation and surface burn.

Adult, male Sprague-Dawley rats were used. Animals were anesthetized and randomly assigned to one of four groups. Groups 1 and 2 received a 20% total body area surface (TBSA) full thickness scald burns while groups 3 and 4 were sham treated. Five hours after burn injury, rats were placed in a nose only exposure device and half of each group was exposured to either room air alone or room temperature tree bark smoke for 16.25 minutes.

Whole body exposure to the chemical warfare agent, mustard gas, bis-(2-chloroethyl) sulfide, or its laboratory model compound, half mustard, 2-chloroethyl ethyl sulfide (CEES), induces cutaneous, respiratory and ocular impairments. Of these, ocular damage causes the most immediate incapacitation with initial symptoms evident within minutes. This incapacitation is a result of irritation and edema of eyelids, conjunctiva and especially cornea. Development of corneal epithelial lesions and edema leads to deterioration of corneal transmissive and refractive properties with untoward effects on visual acuity. Heretofore, there has been no specific pretreatment, or antidotal therapy for mustard gas-induced ocular impairment. In the present study, we describe morphological correlates of the apparent attenuation of such damage by a mixture compound developed by Varma et al. Varma mixture (VM) consists of compounds known to provide bio-energetic support, prevent oxidative stress, modulate membrane permeability and support tissue metabolism. The mustard agent used in this study was CEES.

While sebum provides several functions in the integument, there is considerable interest in the control of excess sebum on the human skin. The primary function of sebum is to lubricate and waterproof the stratum cornenum layer, in addition to preventing hair from becoming brittle. In several cases, the secretion of sebum is inhibited as a result of blockage of the drainage pathway for the sebaceous glands which may result in abnormal skin conduction (1,2). Clinac™ OC (Oil Control) has been developed with a special oil adsorbing polymer, DVB/lsobornyl Methacrylate/Lautyl Methacrylate Copolymer (3). This particular copolymer posses the capacity to adsorb oils because of its high affinity for hydrophobic nonpolar substances. The purpose of this investigation is to show the adsorptive capacity of the acrylate copolymer in Clinac™ OC preparation and in buffer.

The acrylate polymer was incubated in artificial sebum for 4 hrs and 8 hrs at 37 C.

It has been reported that cryptorchidism caused disruption of spermatogenesis that become extensive with time (1). The process of spermatogenesis undergoes spontaneous degeneration in rats, the spermatids degenerate, the primary spermatocytes have been reported to degenerate more commonly (2). Apoptosis has been considered the route for removing sensitive germ cells after short-term experimental cryptorchidism (3). The abdominal heat stress causes cell loss by apoptotic pathway (4). The cellular damage of the experimentally induced cryptorchid adult rat is regulated by local testicular factors in pachytene spermatocyte (5). In this preliminary diagnostic study, we examined the role of the effect of the body temperature on the seminiferous tubule cells in surgically induced unilateral cryptorchid testis at various time periods in rats. This study is to document the extent of the cellular damage at various specified time periods of abdominal retention of the testis.

Despite significant advances in molecular biology and immunology, electron microscopy (EM) continues to be useful for morphologic identification of infectious microbes in body fluid and cultured specimens from humans and experimental animals. Morphologic identification using negative stain and/or thin-section EM is often a primary tool in public health investigations, followed by immunologic, molecular, or cultured isolation. Difficulties encountered are usually related to the length of time between specimen (e.g. stool) collection and preparation for EM and/or handling and shipping conditions. Another negative mitigating factor may be multi-lab interventions prior to arrival. Appropriate specimen collection, storage, and handling prior to attempts to identify the agent are important factors for successful identification.

Barrier-control guidelines called “Universal Precautions for Laboratories“ have for many years been recommended by U.S. and international health services organizations. The guidelines are based on the premise that safe work sites result from a combination of engineering controls, management policies, work practices, and, when required, prompt medical intervention.

Laboratory safety in a diagnostic electron microscopy (EM) laboratory that deals with potentially infectious specimens is a complex issue. The risk of infection of laboratory personnel is an obvious concern, particularly in laboratories, such as diagnostic virology laboratories, which handle infected tissues and body fluids on a routine basis. A second hazard is introduced by the multitude of toxic, corrosive, and irritating chemical reagents required for the preparation of samples for EM. Physical hazards inherent in the complex machinery necessary for EM and other forms of microscopy must also not be overlooked. Attention to each of these concerns must be orchestrated over the course of a multistep process that often lasts several days. Success in this endeavor is facilitated by a comprehensive quality control program encompassing personnel, specimens, chemicals, and equipment.

The foundation for safe handling of samples in the clinical laboratory is the principle of universal precautions, under which all blood, other body fluids, and tissues are considered potentially infectious and handled using appropriate protective measures.

During metamorphosis amphibian tadpoles regress gills, tail and other larval structures. Thus gills are a good model to study how a highly complex three-dimensional vascular network regresses and finally disappears. Presently, only the microvascularization of external gills of larvae of Hynobiusdunni(2) and Litoria ewingi(3) is examined. The present study analyzes the spatio-temporal changes which the gill 3D-vascular network undergoes during metamorphosis using SEM of microvascular corrosion castings and a newly developed 3D-morphometry system (4, 5).

Vascular casts of gills of tadpoles of the South African Clawed Toad, Xenopus laevis Daudin of stages 57 to 62 (6) were analyzed by SEM. Stereopaired images (tilting angle: 6 degrees) grabbed with a slow scan frame grabber (Orion 4.27) from the SEMs photo-display were imported into a 3Dmorphometry system (6) to measure vessel diameters, interbranching distances, branching angles and branching orders of filter row venules. This study reports the changes in the branching orders only.

Vascular corrosion replicas provide unique three-dimensional models of both macro- and microcirculatory angio-architecture. In most replication procedures, blood is initially flushed from the vasculature with a low viscosity, non-clotting medium, such as saline, prior to infusion with the unpolymerized resin. While this removes cellular elements from the vessels and prevents coagulation, the chemical characteristics of the saline and the mode in which it is infused can potentially affect vascular smooth muscle. This can be disadvantageous if subsequent distribution of the resin does not faithfully mimic normal perfusion pathways, or if the vascular lumen is either narrowed due to vasospasm or distended due to excessive intravascular pressure. Alternatively, the composition of the saline can be modified to enhance the replication process. This may be done merely to ensure complete filling of the vasculature or to evaluate anatomical foci instrumental in physiological and pharmacological regulation of perfusion distribution.

The architecture of the kidney of birds (and also reptiles) is, unlike in mammalians, mainly determined by the organization of the blood vascular system. Besides arterial supply and venous drainage, the renal portal system forms a main structural component. While the latter was often regarded as a “primitive” feature in the literature, morphological and physiological data reveal its great functional importance.

Microvascular corrosion casts studied in the scanning electron microscope permit the visualization of minute vessels, retaining their 3D-arrangement. Additionally, when compared with graphical reconstructions of serial sections, this method avoids several inherent artifacts like fixation and dehydration shrinkage as well as the compression of the object by the sectioning blade. Most of the studies on avian kidneys with this technique used the domestic chicken as a model. In order to provide additional material for comparative and functional studies, data on the intrarenal vascular structure of other species are required.

On the basis of ultrastructural, biochemical, cytochemical, and electro-physiological evidence, the stria vascularis, a highly vascular epithelium of the mammalian cochlea, has been implicated as one site of endolymph synthesis. It would seem natural to suspect that its highly developed counterpart in the avian cochlea, the tegmentum vasculosum (TV), might have a similar function. This study utilizes routine light and electron microscopy, biochemistry, cytochemistry, and vascular corrosion casting to describe the structure and blood supply to the (TV) in the duckling and provide evidence for its involvement in endolymph synthesis.

Four to 16 week-old ducklings (Anas platyrhyncos)were anesthetized and anticoagulated and perfused via the common carotid arteries with buffered, 2% glutaraldehyde for routine light microscopy or transmission or scanning electron microscopy, or with Mercox resin for vascular corrosion casting. Casts were macerated in 5% KOH and warm water to remove tissue, cleaned in formic acid and water, dried by lyophilization, mounted on stubs and viewed at 10-20 kv by SEM.

Growth of malignant tumors relies on development of new vessels from the existing vessels, a process called angiogenesis. Little is known about the pattern of chronic vascular growth in the human germ cell testicular cancer. To shed light on this topic, we injected human CRL-2073 testicular cancer cells or saline (sham treated mice) into the testes of SCID-mice and studied the growth of the tumor's vasculature using intravital video microscopy (IVM) on days 7, 14, 21, 28 and 37 after injection. On each day, 4 mice were studied. To better identify microvessels, fluorescein isothiocyanate-dextran (FITC) was injected i.v. prior to IVM. After IVM, one testis was cast with Mercox and studied in a scanning electron microscope (SEM), the other was used for histology. IVM images were transferred to the computer and analyzed using the Lucia morphometry software.

The significance of angiogenesis and the vascular architecture have been stressed in numerous studies of the structure and biological properties of the tumor vasculature and blood flow (Folkman and D'Amore, 1996; Jain, 1988). The important question as to whether the vascular architecture of an individual tumor is tumor type specific has been controversial. This is due, at least in part, to the methodologies used. Most reports confine themselves to qualitative observations and comparisons of gross vascular patterns in host and tumor, or to blood vessel density, length and diameter measurements, which in turn vary with the staining and counting techniques.

We studied the microvascular architecture of four different tumor cell lines (CaX, CaNT, SaS, HEC- 1B) in order to determine whether there is a characteristic vascular pattern for different tumor types and whether it differs significantly from two normal tissues, muscle and gut.

A method for producing plastic castings of the internal structure of hard tissue has been described by Marten et al. (1978). Although they examined dentine, this technique could also be used to examine other hard tissue such as bone (Weber, 1983). The aim of our study is to expose the true threedimensional relationships between the internal structures of the compact bone and these microstructural changes of the mandible in the aging rats.

Nine Wistar male rats were used in this study and divided into 3 groups as follows: 3 weeks-old rats as young stage, 12 weeks-old as adult stage and 80 weeks-old as old stage. All rats were perfused with 2.5% glutaraldehyde via the ascending aorta. In one rat for each group, the mandible was decalcified by 10% EDTA and embedded in paraffin. 10 μm sections were stained with Schmorl’s staining method.

The lung is supplied by pulmonary and bronchial arteries. Unilateral ligation of a main pulmonary artery results in bronchial vascular expansion and new anastomoses between the bronchial and pulmonary circulations. The form and location of this expansion is the subject of this project.

We ligated the left pulmonary of 15 rats and killed 3 rats 1,2,4, 6, and 8 weeks after the ligation. We studied 3 control animals that did not undergo ligation. We cast the vasculature of the lungs with methyl methacrylate and examined both the right and left lungs by light and scanning electron microscopy.

We found that the expansion and anastomoses occurred in and near the bronchovascular bundles and along the pleura, even though the rat pleura is supplied by pulmonary vessels. Near large pulmonary arteries, the junctional and alveolar capillaries were irregular, flattened, and had lateral outbulgings. The diameters varied within short lengths.