Search PubMed⌕ Search

Biomedical subjects

C L Chrisman

Publications and source records attributed to C L Chrisman.

52 records · Page 3Linked to original sources

Effect of maternal parity on aneuploidy in early mouse embryos.

An attempt to evaluate the incidence of chromosomal aneuploidy in mouse blastocysts recovered from females of various ages and parity levels revealed an insignificant regression coefficient for aneuploidy on age of the female and its square, and an insignificant correlation coefficient for aneuploidy with the number of previous offspring born to the dam. However, significant regression coefficients were obtained for aneuploidy on parity of the dam and its square. These results indicate that not only does aneuploidy increase with parity level, but the rate of increase accelerates as parity level increases. Possible explanations for the increase in aneuploidy and its detrimental effect on reproductive efficiency were discussed.

Aneuploidy↗

Investigation of hyperthermia-induced dominant lethal mutations in male mice.

The mutagenic potential of hyperthermia was investigated in a random-bred stock of mice to determine if this is one mechanism by which elevated ambient temperature exerts its deleterious effects on mammalian reproduction. Two dominant lethal assays were conducted to measure mutagenicity during the meiotic and post-meiotic stages of spermatogenesis following various periods of heat stress. Indirect evidence for hyperthermia-induced dominant lethality was obtained in the form of increases in the frequencies of preimplantation loss and sterile matings. However, the large number of sterile matings precluded unambiguous statistical analysis of the incidence of early embryonic mortality that would have provided direct evidence of induced dominant lethality. Control data indicated that the stock of mice used in this experiment is an excellent choice for dominant lethal studies because of the large number of implants and the low frequency of embryonic mortality.

Analysis of Variance↗

Canine intracranial epidermoid cyst.

A 7-year-old intact male pitbull presented with a 2-month history of progressive dysequilibrium. Cerebrospinal fluid analysis was indicative of a central inflammatory or neoplastic disorder. A cerebellar cystic structure was identified on magnetic resonance imaging which was found to be an epidermoid cyst on histopathology.

Animals↗

Magnetic resonance imaging and ultrasonography in the diagnosis of a malignant peripheral nerve sheath tumor in a dog.

A 9-year-old male neutered mixed breed dog had a two-month history of progressive left thoracic limb lameness. There was electromyographic evidence of denervation potentials in all muscles of this limb. In magnetic resonance images a multilobulated, hyperintense mass was visible caudal to the middiaphysis of the left humerus on T-2 weighted images. The mass, which was isointense with surrounding tissue on T1 weighted images, extended proximally towards the brachial plexus. The mass was also visible as a fusiform structure of mixed echogenicity sonographically, although fine-needle aspiration performed at this time was nondiagnostic. A malignant peripheral nerve sheath tumor was diagnosed histopathologically.

Action Potentials↗

Magnetic resonance imaging of spongy degeneration of the central nervous system in a Labrador Retriever.

A 7-month-old, neutered female Labrador Retriever was evaluated for tetraparesis and subtle cerebellar dysfunction. Clinical signs progressed over a period of 6 weeks to severe ataxia, hypermetria, intention tremors, and finally non-ambulatory tetraparesis. On magnetic resonance imaging of the brain there were large, bilaterally symmetrical, ovoid lesions in the region of the deep cerebellar nuclei that were hyperintense on T2-weighted and proton density images and hypointense on T1-weighted images. There were similar but smaller bilaterally symmetrical lesions present within the thalamus. Euthanasia was performed and lesions consistent with the previously described spongy degeneration of Labrador Retrievers were identified. This disease and its relation to similar human heritable leukodystrophies are discussed.

Animals↗

Magnetic resonance imaging of cerebral cortical necrosis (polioencephalomalacia) in a dog.

A 3-year-old neutered female mixed breed dog was examined because of severe, generalized seizure activity, tetraparesis, and encephalopathic signs. Cerebrospinal fluid (CSF) evaluation was unremarkable except for a mild increase in protein. Serum and CSF titers for infectious diseases were negative. Magnetic resonance (MR) imaging examination of the brain was performed and lesions were found within the cerebral gray matter of the temporal and parietal lobes. The lesions had increased signal intensity on T1, T2, and proton density-weighted images. There was mild inhomogeneous enhancement following intravenous contrast medium administration. Neurologic status improved and the seizures were well controlled, but the dog never regained normal mentation and euthanasia was performed 10 weeks after initial evaluation. At necropsy, severe cerebral cortical necrosis was found in the regions corresponding to the lesions seen on MR imaging examination. Large numbers of fat-containing macrophages (gitter cells) were found within these areas, and are thought to be responsible for the characteristic hyperintensity seen on the MR images.

Animals↗

Acute, flaccid quadriplegia in three cats with suspected coral snake envenomation.

Three cats were evaluated for acute, ascending, flaccid quadriplegia; depression; and reduced nociception. Complete or partial neuromuscular junction blockade was found on nerve stimulation studies during electromyographic examinations. Two of the cases had wounds on the chin or paw compatible with coral snake bites. Although a coral snake was found in only one case, coral snake envenomation was suspected because potential for exposure, clinical signs, and electrodiagnostic findings were similar to dogs reported with this condition and to cats with tiger snake envenomation. Only one case received coral snake antivenin. All cases recovered within seven-to-10 days.

Acute Disease↗

Secondary hypoadrenocorticism associated with craniocerebral trauma in a dog.

An 11-month-old, neutered female miniature schnauzer presented with a severe head injury. The dog was treated for the acute effects of craniocerebral trauma and was hospitalized for just over a week. Several weeks later, she became weak and lethargic. A diagnosis of hypoadrenocorticism was confirmed with an adrenocorticotropin hormone (ACTH) stimulation test. An endogenous ACTH assay confirmed secondary hypoadrenocorticism. The dog was tested for hypopituitarism with canine thyroid-stimulating hormone and thyroxine serum assays and an insulin-like growth factor assay. These tests could not confirm panhypopituitarism in this dog. The hypoadrenocorticism was treated with prednisone, and the dog remains controlled adequately three years later.

Adrenal Insufficiency↗

Sensory polyganglioradiculoneuritis in a dog.

Generalized reduction of nociception and conscious and unconscious proprioception were found in an approximately eight-year-old, male, Maltese mixed-breed dog presented for difficulty prehending food and experiencing ataxia of three months duration. Results of needle electromyogram, motor nerve conduction velocity, and cerebrospinal fluid analysis were normal. A diagnosis of sensory polyneuropathy was suspected. No underlying cause could be determined. Neurological signs progressed to quadriparesis over the following four months despite treatment attempts with prednisone and procarbazine. Necropsy confirmed a sensory polyganglioradiculoneuritis, but no inciting cause could be established.

Animals↗

Integration, expression and germ-line transmission of foreign growth hormone genes in medaka (Oryzias latipes).

Gene constructs consisting of human growth hormone (hGH) gene driven by promoter/regulatory sequence of mouse metallothionein (mMT), viral thymidine kinase (vTK), rat cholecystokinin (rCCK), or chicken beta-actin (cBA) gene were injected into the cytoplasm of fertilized medaka eggs via the micropyle. More than 49% of the injected embryos survived at hatching. Up to 26% of the survivors showed integration of the introduced gene construct, as determined by polymerase chain reaction analysis and subsequent confirmation by Southern blot hybridization of the genomic DNA. A significant fraction of F1 progeny, derived from crosses between transgenic founders and the nontransgenic individuals, inherited the transgene. Expression of hGH gene was also observed in some of the P1 founders and F1 transgenic progeny carrying mMT-hCG or cBA-hGH gene. Furthermore, the growth performance of the P1 mMT-hGH and cBA-hGH transgenic founders and F1 cBA-hGH F1 transgenic progeny was significantly greater than their full sibling, nontransgenic individuals. In addition to the microinjection experiment, a gene construct containing the long-terminal repeat (LTR) sequence of avian Rous sarcoma virus (RSV) and rainbow trout (rt) GH2 cDNA was introduced into embryos of medaka by electroporation using an exponential decay electroporator. Approximately 70% of the electroporated embryos survived at hatching, and 20% of the survived individuals integrated RSVLTR-rtGH2 cDNA into their genomes. These two techniques will greatly enhance the ability to study regulation of gene expression in transgenic animals during differentiation and development.

Animals↗