WorldCat Identities

Pierce, Kenneth R.

Overview
Works: 20 works in 22 publications in 1 language and 71 library holdings
Genres: Academic theses  History 
Roles: Author
Classifications: KF3457.3,
Publication Timeline
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Most widely held works by Kenneth R Pierce
The Employee Polygraph Protection Act : a manual for polygraph examiners and employers by F. Lee Bailey( Book )

2 editions published in 1989 in English and held by 30 WorldCat member libraries worldwide

The Employee Polygraph Protection Act of 1988 : a manual for polygraph examiners and employers by F. Lee Bailey( Book )

1 edition published in 1989 in English and held by 14 WorldCat member libraries worldwide

Command and control of corps rear operations by Kenneth R Pierce( Book )

1 edition published in 1986 in English and held by 3 WorldCat member libraries worldwide

This study focuses on Corps Rear Area Operations Center, responsible for command and control of corps rear operations. It recommends the Corps Rear Area Operation Center be combined with the Corps Military Police Brigade and the brigade commander be responsible to the deputy corps commander for rear operations. The study further recommends that the Corps Support Group Rear Operation Center be combined with the Military Police Battalion providing area support to the Corps Support Group
Characterization of the immune response and lesions of the central nervous system in bluetongue virus infection of mice by Lawrence David MacGill( Book )

1 edition published in 1972 in English and held by 3 WorldCat member libraries worldwide

The possibility of the occurrence of a persistent infection of mice with mouse adapted bluetongue virus (MBTV), the pattern of development of the lesions induced in the neonatal mouse brain by infection and some factors responsible for the age dependent immunity to MBTV infection in mice were investigated. Neonatal and weanling mice were inoculated with MBTV to investigate the possibility of their developing a persistent infection. Mice in each age group which survived acute infection were divided into groups of 10 each and one group was killed each month. Brain tissue from these mice was inoculated into neonatal mice in order to detect the presence of MBTV. Tissues from mice in each group were studied utilizing histologic, immunofluorescent, and immunologic techniques. A group of neonatal mice was inoculated intraperitoneally with MBTV in order to study the pathogenesis of cerebral lesions associated with the infection. Inoculated neonates were killed in groups of 4 at various intervals postinoculation and brain tissue was collected from them for examination by histologic, immunofluorescent, and ultrastructural techniques. The data obtained from these studies were used to formulate a hypothesis for the pathogenesis of lesions in the neonatal mouse brain. The initial evidence of neurologic disease was endothelial hypertrophy. This progressed to vascular necrosis, thrombosis, ischemic necrosis (infarction) and invasion of the neuropil with neutrophils.
A histological and ultrastructural study of the pathogenesis of toxic myopathies of avian striated muscle by William Kay Read( Book )

1 edition published in 1968 in English and held by 3 WorldCat member libraries worldwide

Toxic myodegeneration of avian striated muscle was studied by giving intraperitoneal injections of plasmocid[6-methoxy-8-(3-diethylaminopropylamino)quinolone] to 15 chickens and oral doses of ground Cassia occidentalis beans to 20 chickens. Samples of peroneus longus muscle (red fibers), pectoralis superficialis muscle (white fibers), and ventricular myocardium were compared by light microscopy of paraffin-embedded and Araldite-embedded tissue and by electron microscopy. The ultrastructural morphology of fibers of the peroneus longus muscle and the pectoralis superficialis muscle form the control birds was similar to that of human Type I and Type II muscle fibers respectively. The initial lesion in plasmocid toxicity was observed in the sarcoplasmic reticulum of skeletal muscle but not cardiac muscle. Filling of the cisternae of the sarcoplasmic reticulum with a finely granular, electron-opaque material apparently was followed by dilation of these organelles with extreme segmental contraction of individual skeletal muscle fibers. The most severe effect was on the fibers of the peroneus longus muscle. In contrast to plasmocid toxicity, the primary lesion of C. occidentalis poisoning was observed in mitochondria of the myocardium. Dilation and fragmentation of mitochondrial cristae was observed initially and fragmentation of external mitochondrial membranes was seen only in a few mitochondria contain fragments of these cristae. Although these two toxic myopathies were manifested by similar microscopic lesions, initial ultrastructural alterations were distinctly different. It was proposed that the inability of the sarcoplasmic reticulum to transport calcium ions out of the cell fluid in plasmocid toxicity and the alteration of oxidative phosphorylation in C. occidentalis poisoning both result in coagulation necrosis and fragmentation of muscle fibers observed in the terminal stages of toxic myodegeneration
Hereditary striatonigral and cerebello-olivary degeneration of the Kerry Blue Terrier by Donald Lee Montgomery( Book )

1 edition published in 1981 in English and held by 2 WorldCat member libraries worldwide

The character and progression of central nervous system and non-nervous system lesions of a hereditary neurodegenerative disease in the Kerry Blue Terrier were studied in 10 affected dogs ranging in age from 5 to 12 months. Evaluation of the lesions in the naturally occurring disease and comparison of them with those of an experimental animal model indicated a possible pathogenesis for the neuronal degeneration in this disease. Also, this study indicated a possible role for this disease as an animal model for similar diseases that affect man. The present study confirmed the neuroanatomic distribution of neuronal degeneration in the cerebellar cortex (Purkinje cells), caudal olivary nucleus, substantia nigra, and caudate nucleus reported from previous studies and, in addition, revealed neuronal degeneration in the putamen during advanced stages of the disease. The cerebellar cortex and caudate nucleus (and possibly the putamen) were the primary areas of the brain affected while neurodegeneration in the caudal olivary nucleus and substantia nigra was concluded to have resulted from a transsynaptic mechanism.
The United States Army, the Infantry, and national policy 1945 to 1950 by Kenneth R Pierce( Book )

2 editions published in 1978 in English and held by 2 WorldCat member libraries worldwide

An in vitro and in vivo study of the pathogenesis of Mouse Hepatitis Virus-4 infection by John Francis Hansen( Book )

1 edition published in 1980 in English and held by 2 WorldCat member libraries worldwide

The pathogenesis of Mouse Hepatitis Virus-4 (MHV-4) infection was studied in primary confluent murine astrocytic monolayers, murine cerebellar organotypic explants (both during and after the initial period of rapid myelination in vitro), and in the intact weanling mouse. Varying inoculum concentrations of tissue culture adapted virus were used in each of the in vitro studies. Astrocytic monolayers inoculated with a high concentration of virus developed a severe necrotizing cytopathic effect (CPE). A lower concentration of virus resulted in the formation of astrocytic syncytia, cytoplasmic inclusion bodies, and a steady-state infection in which direct cell-to-cell transmission of virus was detected. Immature cerebellar explants inoculated with a high concentration of virus before myelination occurred in vitro developed a necrotizing CPE characterized by necrosis of granule cells and the production of edema. Syncytia and cytoplasmic inclusion bodies also developed within the astrocytic outgrowth. Direct cell-to-cell transmission of virus was detected. Demyelination was located mainly in focal areas of necrosis which were also edematous. Surviving axons were myelinated, or were being myelinated, by 14 days post-inoculation (DPI). Oligodendroglia infrequently had degenerative changed. The low dosage of virus resulted in a milder CPE with the formation of syncytia and inclusion bodies in the astrocytic outgrowth and focal myelin destruction in areas of necrosis. Mature myelinated explants inoculated with a high dosage of virus developed an acute necrotizing CPE which involved all areas of infected explants. The intermediate and low dosages of virus resulted in a CPE which most severely affected the non-neuronal (white matter) areas and was characterized by edema, hydropic degeneration of infected astrocytes, and in explants inoculated with the low viral dosage, primary demyelination and persistent infection in which direct cell-to-cell transmission of virus was detected. Demyelination with the low viral dosage was concluded to be associated with edema which was largely due to the hydropic degeneration of infected astrocytes
Studies on the pathogenesis of the myopathy of coffee senna (Cassia occidentalis) poisoning in rabbits by Peter John O'Hara( Book )

1 edition published in 1970 in English and held by 1 WorldCat member library worldwide

The pathogenesis of the myodegeneration of striated muscles of rabbits poisoned with coffee senna (Cassia occidentalis L.) was studied by use of routine pathological methods. The heart was enlarged due to dilatation of all chambers and the myocardium was pale or yellow. The liver was swollen and appeared mottled due to uniformly distributed pale spots which accentuated the lobular pattern. The thoracic and peritoneal cavities contained serous fluid and strands of fibrin. The microscopic lesions of the hearts of poisoned rabbits were characterized by fine vacuolation of myocardial fibers. The vacuoles were arranged in rows between myofibrils and around muscle nuclei and were the result of swelling of mitochondria and the accumulation of droplets of neutral fat. Swelling of mitochondria was accompanied by a change in the permeability of the mitochondrial membranes. Degeneration of cardiac muscle fibers followed the vacuolation and took 1 of 2 forms. The more common form, myofibrillar degeneration, appeared as a progressive disorganization of myofibrillar A-band patterns. The less common form was hyaline degeneration. An inflammatory reaction characterized by infiltration of small numbers of neutrophils and macrophages and hyperplasia of interstitial fibrocytes occurred in the areas of degeneration but regeneration of cardiac muscle fibers was rarely observed. Myocardial degeneration and congestive cardiac failure produced passive venous congestion of the liver and degeneration of hepatocytes consistent with hypoxic changes. Extensive degeneration of skeletal muscle was found in only 1 rabbit which had been given a large total dose of coffee senna. The response of skeletal muscle fibers of poisoned rabbits to a mild crushing injury was similar to the response of control rabbits. The predominant form of regenerative response to this injury in control and poisoned rabbits was discontinuous regeneration which was virtually complete in 10 days. Continuous regeneration was apparent for up to 30 days in areas of cicatrization or residual necrotic debris
A comparative examination of accounting and economic concepts of enterprise income by Kenneth R Pierce( )

1 edition published in 1965 in English and held by 1 WorldCat member library worldwide

Toxicity Testing of Antimalarial Drugs in Swine. I.A Study of Quinine Sulfate Toxicity( Book )

1 edition published in 1967 in English and held by 1 WorldCat member library worldwide

Quinine sulfate administered orally to swine in doses of 361 mg/kg/day (milligrams/kilograms/day) resulted in an LD 100/10 (Lethal dose 100/10), whereas, 180 mg/kg/day produced death in one of four pigs in 30 days, and no ill effects were observed in animals that received 45 mg/kg/day for 30 days. The most consistent symptoms observed were: emesis, depression, ataxia, partial to complete loss of sight and convulsions. The hematologic and biochemical results were very unimpressive, with few changes. The significant gross lesions may be summarized as: a hemorrhagic disorder, corneal lesions and alopecia. The most significant microscopic lesions are vacuolization of neurons, corneal lesions, bone marrow lesions and degenerative lesions of the arteriolar walls. Keywords: U/A Reports, Toxicity, Antimalarial, Drugs, Swine, Testing, Pharmacology, Quinine sulfate, Medical research. (jg)
A study of the biochemical and morphological changes in GM₂-gangliosidosis of Yorkshire swine and the influence of chloroquine HCL upon these changes by Stanley Dwight Kosanke( Book )

1 edition published in 1975 in English and held by 1 WorldCat member library worldwide

The biochemical and morphological characteristics of porcine cerebrospinal lipodystrophy in different stages of development were ascertained and were compared to corresponding characteristics of the human GM₂-gangliosidoses. The study was divided into 2 separate experiments. In the 1st experiment 11 control (normal and carrier) and 14 affected Yorkshire pigs were used to investigate the pathogenesis of the fundamental cellular lesion by evaluating the progression of the basic biochemical (enzyme and ganglioside assays) and morphological (neuronal and glial) changes in the central nervous system. Tissues were collected from pigs killed at 1 day (newborn or stillborn) to 175 days of age. The purpose of the 2nd experiment was to evaluate the effect of chloroquine HCl on lipodystrophic pigs. Chloroquine HCl was given to 4 control and 4 affected pigs at the rate of 2.5 mh/Ib/day, and to 1 control and 1 affected pig at the rate of 7.5 to 10.0 mg/Ib every other day. Control and affected pigs used in each experiment were identified on the basis of the level of N-acetly-B-D-hexosaminidase activity in serum and in leukocyte, liver, and brain homogenates. Total N-acetyl-B-D-hexosaminidase values in the tissue homogenatcs were lower in affected than in control, while serum total N-acetyl-B-D-hexosaminidase levels were higher in the affected pigs than in either the carrier or normal pigs. The serum enzyme assay was found to be a reliable test to distinguish carrier pigs, with moderate serum levels of activity of this enzyme, from the normal pigs which had the lowest level of enzyme activity in the serum. Two consistent features of all affected pigs were the presence of diffuse grayish-white spots in the retinas examined either stereomicroscopically or ophthalmoscophically, and prominent granules in the cytoplasm of most neutrophils and lymphocytes stained with Wright-Giemsa stain
Toxicity testing of antimalarial drugs in swine and dogs( Book )

1 edition published in 1969 in English and held by 1 WorldCat member library worldwide

Acute, subacute, and chronic toxicity studies and photosensitization studies were conducted in swine and dogs using antimalarial compounds singularly or in combination. The subcutaneous administration of WR-9838-B, 5 mg/kg or 10 mg/kg, for 15 consecutive days resulted in clinical manifestations of lameness, loss of weight and appetite, ocular involvement and swelling at injection sites. The oral administration of WR 40,070 for 28 consecutive days resulted in clinical manifestations of vomition, excessive salivation and hyperirritability. Healthy purebred beagle dogs were given a combination of chloroquine and trimethoprim orally in an 'Acute Minimum Lethal Dose Study' and in a 'Subacute Toxicity Study.' The symptoms observed included emesis, depression, incoordination, ataxia, convulsions and death. The minimum amount of the following antimalarial compounds required to consistently produce phototoxicity in white swine, when four doses were administered orally during 44 hours of U.V. light exposure was: quinine sulfate, 25 mg/kg; WR-7930, 15 mg/kg; and WR-30090, 25 mg/kg. Specific-pathogen-free swine were given a combination of chloroquine, primaquine, and D.F.D. orally, twice weekly for four weeks
The lymphoreticular response of intact and immunologically altered dogs to infection with Ehrlichia canis by Michael James Reardon( Book )

1 edition published in 1977 in English and held by 1 WorldCat member library worldwide

The lymphoreticular response of dogs to Ehrlichia canis infection was studied in immunocompetent dogs (Group I) and in dogs after immunosuppressive therapy with cyclophosphamide (Group II) or antilymphocyte serum (Group III). Immunosuppression did not increase the mortality rate nor did it prevent the clinical manifestations of acute ehrlichiasis. Anorexia, pyrexia, weight loss and mucopurulent ocular-nasal discharge were consistent features of the acute infection. Hypergammglobulinemia was consistently observed in Group I principals but was less pronounced in Group II principals and absent in the principals of Group III. A similar trend was observed in anti-E. canis IFA titers although very low titers were observed in some Group III principals. Gross lesions consisted of heavy dense lungs, slightly pale livers, splenomegaly and an increased amount of red, active-appearing long bone marrow in Group I principals. Only the red active-appearing long bone marrow was prominent in the other groups. Hemorrhagic cystitis due to cyclophosphamide was observed in all Group II dogs. Previously unreported microscopic lesions observed in Group I principals were marked hyperplasia of the thymic dependent areas of spleen and lymph nodes, parafollicular splenic hemorrhages, phlebitis and perivasculitis in the renal cortex involving especially the stellate veins and proliferative RE nodules in the liver causing necrosis of adjacent hepatocytes. Group II and III principals had less severe lesions and those that occurred appeared later in the course of the disease
The pathogenesis of sodium chloride toxicity in the young chicken by Wallace Brown Baze( Book )

1 edition published in 1985 in English and held by 1 WorldCat member library worldwide

Sodium chloride(NaCl) toxicity was induced in two-week old chickens given either 1% or 1.5% NaCl in the drinking water. Chickens given 1.5% NaCl developed a severe encephalopathy characterized clinically by depression, ataxia, seizures and death with a median survival time of 5 days. Clinicopathologically, affected chickens had significant increases in serum sodium (204.8[plus or minus]16 vs 141.7[plus or minus]2.3 mEg/l in controls), chloride (176.6[plus or minus]14 vs 108.5[plus or minus]2.6mEq/l in controls) and osmolarity (422[plus or minus]27 vs 306.4[plus or minus]5.5m0sm/kg in controls) and pathologically had spongiform degeneration (status spongiosus) of the grey and white matter, degeneration of putative oligodendroglia and splitting (separation) of myelin sheaths, apparently at the intraperiod line. The encephalopathy was similar to the lesions associated with certain other intoxications effecting the central nervous system (e.g. tetraethyl tin, hexachlorophene, lead and the intoxication in man associated with deranged serum sodium causing central pontine myelinolysis). The NaCl induced encephalopathy was proposed to most likely have resulted from a direct toxic effect of Na+ or NaCl on oligodendroglia and/or the myelin sheath. Chickens given 1% did not develop clinical signs of encephalopathy but did have mild clinicopathologic and pathologic lesions that were comparable to chickens given 1.5% NaCl. To further explore the mechanism of the NaCl induced encephalopathy, young chickens administered 1.5% NaCl in the drinking water were given either dexamethasone (corticosteroid) or ethacrynic acid (nonosmotic diuretic) which are compounds used to reduce or prevent the development of cerebral edema. Dexamethasone (40mg/kg/day), known to stabilize membranes of the blood-brain barrier and stimulate electrolyte shifts in the CNS of mammals, had no beneficial effect and actually enhanced the severity of the salt toxicity (reducing the median survival time from 5 to 2 days). The mechanism of this enhancement was possibly the result of corticosteroid induced sodium and water retention or cardiopulmonary complications. Ethacrynic acid (0.1mg/kg/day), previously shown to block Cl- transport and possibly Na+ and water across cell membrane in mammals, had no significant effect on the encephalopathy and exacerbated the toxicity when given at higher concentrations. No definitive explanation was found for the enhanced toxicity but a toxic metabolite or direct interaction of the drug with NaCl was considered
A morphological and biochemical study of the pathogenesis of ovine hepatic fatty cirrhosis by L. Garry Adams( Book )

1 edition published in 1968 in English and held by 1 WorldCat member library worldwide

Ovine hepatic fatty cirrhosis (HFC) was found to be a noninfectious chronic progressive disease of the liver, characterized macroscopically by various amounts of fatty degeneration, cirrhosis and compensatory hypertrophy. The disease occurred in five West Texas counties and was clinically characterized by a long subclinical course, gradual weight loss, ascites, emaciation, debilitation and hepatic coma. Microscopically, the affected hepatocytes underwent a sequence of pathological changes described as follows: cytoplasmic distension with small lipid droplets, coalescence of the small lipid droplets to form large lipid spherules, rupture of cytoplasmic septa between contiguous hepatocytes by intracellular pressures apparently due to enlarging lipid spherules, formation of fatty cysts around large lipid spherules, dissolution of fatty cysts, condensation of hepatic reticulin and proliferation of fibrous connective tissue. Ceroid was found in the liver, lung, spleen and the hepatic and posterior mediastinal lymph nodes. The fundamental lesion of HFC was an abnormal accumulation of intrahepatocytic lipid with fibrosis apparently occurring only when the amount of accumulated lipid was enough to rupture hepatocytes and form fatty cysts. The relationship between the pathological lesions of HFC and nutritional cirrhosis was revolved.
Down the Rabbit Hole : who decides what's arbitrable by Kenneth R Pierce( )

1 edition published in 2004 in English and held by 1 WorldCat member library worldwide

A study of the pathogenesis of the peripheral neuropathy of experimental coyotillo (Karwinskia humboldtiana), poisoning in goats by Kenneth Mervyn Charlton( Book )

1 edition published in 1970 in English and held by 1 WorldCat member library worldwide

The pathogenesis of coyotillo (Karwinskia humboldtiana) neuropathy was studied in 26 goats. Twenty-two goats were poisoned with daily oral doses of ground coyotillo fruits, and 4 goats were maintained as controls. Fourteen goats received daily doses of 0.05 per cent, 6 received daily doses of 0.04 per cent, and 2 received daily doses of 0.01 per cent of their body weights. Most of the goats given 0.05 or 0.04 per cent of their body weights were dosed for 6 or 7 days, one of the 2 goats given doses of 0.01 per cent was dosed for 66 days and the other for 69 days. They were killed at various times after their first dosing day. Clinical and neurophysiologic studies included examination of the clinical signs, elicitation of various reflexes, and determination of nerve condition velocity.
A study of the pathogenesis of Mycoplasma synoviae infections by Donald Mark Sells( Book )

1 edition published in 1971 in English and held by 1 WorldCat member library worldwide

The pathogenesis of the lesions of Mycoplasma synoviae infections was studied in vivo and in vitro. The in vivo studies consisted of a study of the microscopic lesions of M. synoviae infected chickens at 8, 18, 28, 38, and 48 days postinoculation. The lesions in the non-bursectomized infected chickens were compared with those in infected chickens which were bursectomized by the inoculation of testosterone proprionate into their embryonic stages in eggs. Erythrocytic and leukocytic concentrations in blood and serum M. synoviae agglutination titers developing in bursectromized and non bursectomized infected and control chickens were compared. Total serum protein concentrations, electrophoretic patterns of serum proteins and rheumatoid factor titers of the non-bursectomized infected and control chickens were evaluated. The effects of M. synoviae on myocardial explants grown in vitro, the effects of sensitized lymphocytes on infected myocardial explants and the effects of immune serum and complement on infected myocardial explants were investigated.
A study of the pathogenesis of cardiac lesions in gnotobiotic chickens infected experimentally with Mycoplasma synoviae by Kirklyn McNeer Kerr( Book )

1 edition published in 1970 in English and held by 1 WorldCat member library worldwide

The pathogenesis of cardiac lesions associated with Mycoplasma synoviae-infection in gnotobiotic chickens was studied. Three separate groups, consisting of 24, 23 and 25 gnotobiotic chickens, were hatched from specific-pathogen-free eggs and maintained in plastic-film, controlled-environment isolators using techniques for handling germfree animals. When two-weeks-old, each chicken in Group I was injected in the left foot pad with 10 times the EID₅₀ of a yolkallantoic culture of Mycoplasma synoviae. Each chicken in Group II was given 10,000 times the EID₅₀ at the same time. Chickens in Group III served as uninfected controls. Separate groups of 4 chickens from Group I, 2 to 5 chickens from Group II and 4 to 5 chickens from Group III were killed 5, 10, 15, 20, 25 and 30 days postinoculation. Specimens were collected from each chicken on each sampling day for hematology, enzymology, gross pathology, histopathology, electron microscopy, microbiology and serology. Data from these various studies were used to formulate a hypothesis on the pathogenesis of cardiac lesions and to evaluate the sequential development and nature of other lesions in infected chickens. A severe anemia, which was characterized as hemolytic, macrocytic and normochromic to hypochromic, developed in infected chickens. Anemia was more severe in chickens from Group II. Infected chickens had a leucocytosis due to heterophilia and monocytosis. Infected chickens had a cardiomegaly and the magnitude of the increase in relative heart weight was correlated with the increase in severity of the anemia
 
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