Primary Site Of Damage Research Articles

Anatomical effects of intense tone stimulation in the goldfish ear: Dependence on sound‐pressure level and frequency

The final results of an experimental investigation to study the extent of frequency regionalization in the ear of goldfish are presented. Goldfish about 6 in. in body length were subjected to intense tones at 250 and 500 Hz, and four different sound‐pressure levels. They were placed in a waveguide and constrained as close as possible to a pressure antinode so that the primary response of the inner ear was due to the induced motion of the swimbladder and Weberian ossicles. Both saccular and lagenar maculae were examined under a scanning electron microscope to determine the location and extent of hair cell damage as a function of frequency and sound‐pressure level. The results are not inconsistent with the gross frequency regionalization in the saccular macula of codfish determined by P. S. Enger [Hearing and Sound Communication in Fishes (Springer, New York, 1981), pp. 243–255]. In addition, the results indicate a possible breakdown of the Weberian apparatus at extremely high sound‐pressure levels where the primary site of damage switches from the saccule to lagena. This is consistent with the behavior of the system based on its viscoelastic properties as postulated by R. McN. Alexander [J. Exp. Biol. 38, 747–757 (1961)]. Work supported in part by ONR and NIH.]

Immunization of cattle against Boophilus microplus using extracts derived from adult female ticks: Histopathology of ticks feeding on vaccinated cattle

Immunization of cattle against Boophilus microplus using extracts derived from adult female ticks: histopathology of ticks feeding on vaccinated cattle. International Journal for Parasitology 16: 35–41. Histological examination of the tick Boophilus microplus fed on cattle vaccinated with tick extract showed that the gut was the primary site of damage. Within 24–48 h of attachment digest cells were either sloughed off into the lumen or were completely destroyed leaving only the basal lamina and muscle layer. Subsequent rupture of the gut allowed host leucocytes to enter the haemocoel and attack other tissues. After 6 days the surviving ticks showed a delay in development of digest cells and gut basophilic cells. Many host leucocytes had escaped into the haemolymph and these cells destroyed tick muscle and Malpighian tubules but not salivary glands. Females which survived to post-engorgement also had damaged gut cells. In males the histopathology of the gut was similar but the accessory gland of the reproductive organ was also damaged by host leucocytes. These effects on feeding ticks were not found on control cattle and have not been reported on animals with naturally acquired resistance to tick infestations. Vaccination apparently stimulated a different mechanism of resistance to ticks.

Cerebral photosensitisation by haematoporphyrin derivative. Evidence for an endothelial site of action.

Exposure of the cranium to white light in mice that had been given haematoporphyrin derivative (HpD) led to a rapid onset of vasogenic cerebral oedema, cerebral necrosis, coma and death. Selectivity of the initial damage for endothelium was suggested by (a) early breakdown (less than 1 h) of the blood-brain barrier (BBB) as shown by increased permeability to Evans blue (b) separation and increased vesiculation of endothelial cells at 2 h and (c) endothelial cell pyknosis at 3--4 h in small vessels next to apparently undamaged neurones and neuroglia. There was no damage to myelin sheaths, and astrocytes showed only end-feet oedema, a reaction to exudation of protein-rich fluid. Within a few hours of illumination, most cells in the illuminated area were necrotic. Cerebral photosensitivity persisted for at least 12 weeks after a single injection of HpD. Our results suggest that the primary site of damage in the brain is the endothelium of small vessels, and that HpD remains associated with this for a remarkably long time. These findings are relevant to the mechanisms by which photodynamic therapy damages other tissues, including neoplasms, and particularly to the possible application of this treatment to brain tumours.

Photoacoustic and fluorescence measurements of the chilling response and their relationship to carbon dioxide uptake in tomato plants

The response of tomato plants to various chilling treatments was studied using two approaches for the measurement of photosynthetic activity. One involved the use of a portable fluorometer for the measurement of in-vivo chlorophyll fluorescence, while the other employed a newly introduced photoacoustic system which allowed changes in oxygen evolution to be followed in a leaf disc. A strong correlation was found between results obtained by each system and those obtained by a conventional open gas-exchange system for the determination of CO2 uptake. Both systems of measurements could readily distinguish between the effects of chilling in the dark (at 3° C for 18 h) and chilling at high photon flux density (2000 μmol m(-2) s(-1) for 5h at 5° C). Chilling in the dark had practically no effect on the quantum yield of oxygen evolution, chlorophyll fluorescence or CO2 uptake, while chilling at excessively high photon flux density resulted in a sharp reduction (50-70%) in the quantum yields obtained. The results support the view that photosystem II cannot be the primary site of damage by chilling in the dark, although it is significantly affected by chilling at high light intensity.

Management of Brown Recluse Spider Bite-Reply

<h3>In Reply.—</h3> Based on previous experience in an endemic area and our report, Dr Berger questions whether dapsone is indicated for severe brown recluse spider "bites." We agree that (1) not all "bites" should be treated¹; (2) in experimental loxoscelism, blood vessels were the primary site of damage; and (3) polymorphonuclear leukocytes (PMNs) were required for extensive cutaneous necrosis.²We also point out that in humans, extensive PMN accumulation and perivasculitis are routinely noted 24 to 72 hours after the bite and<i>before skin necrosis</i>(personal observations³). These findings have diagnostic and prognostic implications. In humans, once skin necrosis occurs, lesions persist for weeks. The goal of dapsone therapy is to decrease the ulcerated bite size and speed resolution. In experimental animals, any therapy such as dapsone or specific antivenom that reduced inflammation and PMN infiltration proportionately reduced cutaneous morbidity. Persistent inflammation in bites has been studied

Amyloid neuropathy in multiple myeloma and other plasma cell dyscrasias: A hypothesis of the pathogenesis of amyloid neuropathies

The development of amyloid neuropathy is an uncommon complication of multiple myeloma. The clinical, electrophysiological and pathological features of 3 such patients are described. The small fiber neuropathy in these 3 cases was similar to that in patients with primary amyloidosis and with the Andrade-type of familial neuropathy, and differed from the large fiber neuropathy which more commonly develops in patients with multiple myeloma. We advance the hypothesis that the absence of the blood-nerve barrier in the dorsal root and sympathetic ganglia allows the access of amyloidogenic proteins to these ganglia, and that these ganglia are the primary site of damage to the peripheral nervous system in the amyloid neuropathies.

Ultrastructure of the esophageal muscle in achalasia and diffuse esophageal spasm.

The pathogenesis of dysphagia in achalasia and diffuse esophageal spasm (DES) is not understood completely, and the primary site of damage in these two entities is not known. This project was undertaken to study the ultrastructural changes present in the muscular wall of the esophagus in eight patients with achalasia and nine patients with DES, compared with seven controls. The ultrastructural alterations in the smooth muscle of all patients were neither pronounced nor consistent. However, nonspecific changes, including filament disarray, mottling of the fiber density in myocytes, thick and long cytoplasmic dense bodies, long dense plaques, and few nexus junctions were seen in both achalasia and DES. In addition, the smooth muscle cells in achalasia exhibited nuclear and cytoplasmic inclusions. Statistical analysis of the number of muscle cells per unit area suggested that the gross thickening of the muscular wall of the esophagus in cases of DES is because of hyperplasia and not hypertrophy of muscle cells. A striking change seen in achalasia esophagi and a few cases of DES, as compared to the controls, was the marked loss of small nerve fibers and the paucity of granules in the remaining fibers. This study points to a neurogenic pathogenesis for dysphagia in achalasia with secondary nonspecific changes in the smooth muscle in these two diseases. No nerve abnormalities were noticed in DES.

Fertilizing capacity and ultrastructure of fowl and turkey spermatozoa before and after freezing

The fertilizing capacity, motility and ultrastructure of fowl and turkey spermatozoa were examined at various stages of the freezing process. For both species, fertility and motility were depressed after equilibration with dimethyl-sulphoxide at 5 degrees C. After freezing, motility was maintained at 55% for fowl spermatozoa and 40% for turkey spermatozoa; however, fertility was 55% for the fowl and 0% for the turkey. Qualitatively, the damage to the spermatozoa of both species was nearly identical, as revealed by scanning and transmission electron microscopy. The plasmalemma was the primary site of damage. 'Bent' spermatozoa, coiled tails and swollen mitochondria were also present. Damage to the acrosome was only observed in spermatozoa which had been frozen to -180 degrees or -196 degrees C. These changes were attributed to adverse osmotic conditions. Binding of cationic ferritin to the plasmalemma of spermatozoa from both species remained unaltered.

Banding pattern analysis of initial structural chromosome alterations induced by N-methyl- N′-nitro- N-nitrosoguanidine in Syrian hamster cells

Cultured secondary Syrian hamster embryo cells exposed to 0.5 N-methyl- N′-nitro- N-nitrosoguanidine (MNNG) μg/ml medium exhibited chromatid type of aberrations consisting of gaps, breaks and exchanges. Although no specific chromosome or chromosome segment was preferentially affected, chromosomes belonging to the larger groups tended to more often involved. G-band analysis demonstrated that 80% of the lesions occured in negative bands, 9% involved the centromere, 3% were on non-banded heterochromatin, and approximately 8% of the lesions could not be definitely categorized by G-band analysis. Whether the lesions occur at positive bands or at the interface between negative and positive bands is difficult to discern by the G-band resolution. The Y chromosome compared to autosomes of similar size rarely had lesions. X chromosome damage was found in both the euchromatic and heterochromatic arms. However, both sex chromosomes, as well as an autosome (E20) which is heterochromatic on its long arm, were not found joined to the chromatids of other chromosomes, further emphasizing that chromosomes with large heterochromatic areas are isolated in terms of chromatid exchange events. The analysis of MNNG induced chromosome damage indicates that the negative bands are the primary site of damage and points of exchange.

The role of the centriolar region in animal cell mitosis. A laser microbeam study.

An argon ion laser microbeam (488 and 514 nm) was used to selectively irradiate one of the two centriolar regions of rat kangaroo Potorous tridactylis (PtK2) prophase cells in vitro. The cells were sensitized to the laser radiation by treatment with acridine orange (0.1-0.2 mug/ml). Ultrastructural examination of the irradiated centriolar regions demonstrated that the primary site of damage was the pericentriolar material. This result suggests that nucleic acid is present in the pericentriolar material. Behavioral and ultrastructural analysis demonstrated that cells with one damaged pericentriolar zone could undergo (a) nuclear membrane breakdown, (b) chromosome condensation, (c) metaphase plate formation, and (d) cytokinesis. However, the chromosomes neither separated nor exhibited any anaphase movements. Detailed ultrastructural analysis revealed the presence of kinetochore microtubules on both sides of chromosome mass and a lack of microtubules in the cytokinesis constriction. These results indicate that the pericentriolar material is important in spindle orgainization and essential for the formation of the interpolar microtubules.

Types of Genital Prolapse

When supporting tissues of the birth canal are weakened, genital prolapse may occur. Prolapse is seen as a manifestation of upper vaginal inversion, lower vaginal eversion, or both. The rate of progression may give clues to etiology and prognosis, but the physician must determine the site of primary damage. Only repair of the primary weakness can stem progression and prevent recurrence.

The failure of 109Cd to traverse spermatogenic pathway.

Wetterdal (1958) showed that zinc, an element essential for spermatogenesis, is incorporated into developing spermatogenic elements within the testis. Cadmium, physico-chemically similar to zinc, causes selective destruction of the testis; administration of zinc prevents cadmium damage (Parizek, 1957; Kar, Das & Mukerji, 1960; Gunn, Gould & Anderson, 1961). Parizek (1960) suggested that cadmium exerts testicular injury by displacing zinc from its natural sites in seminiferous tubules and that the haemorrhagic reactions, so characteristic of cadmium injury, are a secondary effect. More recent evidence indicates that the vascular endothelium of the testis is the primary site of damage and that necrosis of parenchyma follows secondarily (Gunn, Gould & Anderson, 1963a; Chiquoine, 1964; Mason, Brown, Young & Nesbit, 1964; Niemi & Kormano, 1965; Waites & Setchell, 1966). The following experiments were initiated using radio-isotopes to determine

Mode of Action of Prymnesium parvum Ichthyotoxin

SYNOPSIS. The mechanism of Prymnesium parvum ichthyotoxicity was studied in immersed minnows (Gambusia affinis) in the presence of various synergists (especially polyamines and invert soaps) and under varying conditions of pH and salinity. The effect of immersion in toxin‐synergist solution on permeability of gill tissues to trypan blue and to radioactive substances, e.g., I125 and radio‐iodinated albumin, was established. Fish sensitivity to various toxic substances was increased after immersion for short periods in suitable toxinsynergist solutions. This sensitivity, as well as the increased permeability of gill tissue, was transient and disappeared when fish were stored in tap water for several hours after the toxin‐synergist treatment. Good correlation was found between the conditions (synergist quality and concentration, pH, salinity) leading to P. parvum ichthyotoxicity and conditions instrumental in increased gill permeability and toxin sensitivity. The primary site of damage is concluded to be the gill membrane.

Iodine-Induced Submandibular Sialadenitis in the Hamster

SummaryAdministration of large amounts of potassium iodide to the hamster leads to an inflammatory reaction in the submandibular glands, but not in the parotid or sublingual structures. The primary site of damage is the distal duct system. Such selective damage by this agent may be related to the greater concentrating ability of iodine by the submandibular glands in contrast to the parotids and sublinguals.

GUILLAIN-BARRÉ SYNDROME ("INFECTIOUS POLYNEURITIS") AND ACUTE ANTERIOR POLIOMYELITIS

Since Guillain, Barre and Strohl1described a peculiar form of polyneuritis coexisting with normal cell count and increased protein of the cerebrospinal fluid, considerable attention has been devoted, particularly in the pediatric literature, to the problem of differentiation between this type of polyneuritis and acute anterior poliomyelitis. There appears to be a consensus that the two diseases are entirely distinct. However, from the etiologic point of view this contention lacks convincing evidence; in fact, the causative agent of the Guillain-Barre syndrome is still unknown; and, curiously, no attempts have been made to ascertain whether poliomyelitic virus can be isolated from patients affected with this type of polyneuritis. From a pathologic point of view, a distinction between the two conditions seems justified. In infectious polyneuritis the primary site of damage is in the peripheral nerves and spinal ganglions, in contradistinction to the involvement of the anterior horn in poliomyelitis. Pathologic