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Biomedical subjects

K A Collins

Publications and source records attributed to K A Collins.

At least 55 records · Page 3Linked to original sources

The antinociception induced by beta-endorphin administered intrathecally is mediated by the activation of mu- and kappa-opioid receptors in the rat.

The antinociception induced by beta-endorphin given supraspinally has been previously demonstrated to be mediated by the stimulation of epsilon-, but not mu-, delta- or kappa-opioid receptors in rats and mice. The present study was designed to determine what types of opioid receptors in the spinal cord are involved in the antinociception induced by intrathecally (i.t.) administered beta-endorphin. Antinociception was assessed by the tail-flick test in male Sprague-Dawley rats. CTOP (0.9-6.6 nmol), a selective mu-opioid receptor antagonist, or nor-BNI(13.6-95.3 nmol), a selective kappa-opioid receptor antagonist, given i.t. dose-dependently reversed i.t. administered beta-endorphin-induced inhibition of the tail-flick response. On the other hand, naltrindole (6.6-44.4 nmol), a selective delta-opioid receptor antagonist, or beta-endorphin (1-27) (1-6.7 nmol), a selective epsilon-opioid receptor antagonist given i.t., did not antagonize the inhibition of the tail-flick response induced by i.t. administered beta-endorphin. The results are consistent with the previous study in mice [Tseng LF and Collins KA (1992) Eur J Pharmacol 214: 59-65] that the antinociception induced by beta-endorphin given i.t. is mediated by the stimulation of mu- and kappa-, but not delta- and epsilon-opioid receptors.

Animals↗

Identification of male epithelial cells in routine postcoital cervicovaginal smears using fluorescence in situ hybridization. Application in sexual assault and molestation.

In a prospective blinded controlled study, the efficacy of fluorescence in situ hybridization (FISH) to detect non-sperm male cells verifying sexual contact was examined. Cervicovaginal smears (CVS) from 40 women with reported post-coital intervals were examined for sperm by cytology and for sperm and non-sperm male cells by FISH using X and Y chromosome specific DNA probes. Fluorescence in situ hybridization identified sperm and/or non-sperm male cells in all specimens from women with positive coital histories, including when the partner had a vasectomy. Male cells were also detectable by FISH in CVS up to 3 weeks after coitus. In comparison, cytology identified sperm in 41% of the positive coital history cases, and none beyond 2 weeks. Fluorescence in situ hybridization is highly sensitive and specific in detecting male cells, and can be performed rapidly on routine CVS. Application of this technique can provide new and additional evidence of sexual contact when current tests are inconclusive.

Coitus↗

Intercellular adhesion molecule 1 (ICAM-1) and bcl-2 are differentially expressed in early evolving malignant melanoma.

The expression of intercellular adhesion molecule 1 (ICAM-1), a molecule pivotal in many inflammatory and immune paracrine interactions, has been highly correlated with malignant melanoma (MM) progression. Because numerous parallels exist between tissues of neural crest origin and the immune system in the regulation of postmitotic cell survival, ICAM-1 expression was studied in MM and compared with that of B-cell lymphoma/leukemia 2 protein (bcl-2 oncoprotein), an important regulator in prolonging lymphoid cell survival by blocking programmed cell death. Frozen sections from 33 cases were studied by immunoperoxidase techniques: 14 primary MM (five in situ), nine metastatic MM (one epidermotropic), four melanocytic nevi, and six normal skin controls. The percentages of the cells that stained and their intensities (0-4+) were graded. Both ICAM-1 (90%, 3-4+) and bcl-2 (95%, 2-4+) were strongly expressed in all nine metastases, including the epidermotropic disease extension. Bcl-2 strongly decorated the tumor cells in all 14 cases of primary MM (80%, 2-4+); in the five in situ MM, bcl-2 stained the atypical melanocytes at the dermal-epidermal junction (DEJ) and throughout the epidermis (75%, 1-2+). In contrast, ICAM-1 was negative in the in situ MM. ICAM-1 expression became strong (85%, 2-4+) in the dermal component of early invasive disease. Both ICAM-1 and bcl-2 were expressed in melanocytic nevi, decreasing in intensity deep within the dermis as the nevus cells senesced ("matured"). Only bcl-2 was expressed in the normal melanocytes of the six skin controls. These data show that bcl-2 is constitutively expressed in normal melanocytes and melanocytic nevi and persists in the transformed cells of early and late MM. ICAM-1 is expressed only after dermal involvement occurs, both in melanocytic nevi and in invasive MM; it persists in metastatic disease. The coexpression of bcl-2 and ICAM-1 demonstrates another similarity between the immune and neural crest systems, but it does not define or necessarily imply any functional interaction between the two proteins. The intercellular relationship of these two molecules, if any, remains to be investigated.

Apoptosis↗

Death by bull-edger. An unusual homicide using a woodworking implement.

Impulsive killers often use whatever instrument is close at hand in the perpetration of their deed. We describe a homicidal death, first thought to be accidental, in a rural sawmill where the assailant manipulated a large board of wood into a machine known as a bull-edger (which cuts logs into rough boards) in such a fashion as to cause the death of his work partner. The physics of the events at the scene as well as the subsequent investigation are discussed.

Accidents, Occupational↗

Angiotropic large cell lymphoma.

Lymphomas are malignant neoplasms of cells native to lymphoid tissue that can arise anywhere in the body. Angiotropic large cell lymphoma (ALCL) is characterized by a proliferation of neoplastic mononuclear cells within the lumina of small blood vessels. The clinical manifestations are usually neurologic, including progressive dementia and nonlocalizing deficits, cutaneous infiltration, adrenal masses, or fever of unknown origin. The diagnosis is made at autopsy or on skin biopsy, brain biopsy, or other surgical resection. Differential diagnoses include metastatic malignant neoplasms and vascular tumors. We report the case of a 63-year-old white man who had neurologic signs and symptoms as well as dyspnea. Autopsy revealed ALCL involving multiple organ systems, including the central nervous system. Diagnostic techniques currently used to confirm the nature of this malignant neoplasm include immunohistochemistry, ultrastructural analysis, cytogenetics, and molecular biologic studies.

Brain↗

The cytologic evaluation of lipid-laden alveolar macrophages as an indicator of aspiration pneumonia in young children.

Gastroesophageal reflux with aspiration of feedings in infants and young children may be involved in the development of chronic lung damage. Our laboratory has utilized tracheal aspirates stained with oil red O to identify and quantitate lipid-laden alveolar macrophages as a marker of such aspiration. During the last 10 years, we have evaluated 244 tracheal aspiration smears in children. Although a few patients were up to 3 years old, the vast majority were infants. The cytologist looked for the presence of and the number of oil red O-positive macrophages on tracheal aspirate smears. The specimens were easily assigned grades of absent (grade = 0), low positive (grade 1: 1-25 lipid-laden macrophages), moderate positive (grade 2: 26-50 lipid-laden macrophages), and high positive (grade 3: > 50 lipid-laden macrophages). The grade was then correlated with the positive or negative clinical diagnosis of gastroesophageal reflux with aspiration. We believe the cytologic evaluation and grading of oil red O-stained tracheal aspirates for lipid-laden macrophages is valuable in identifying these patients with gastroesophageal reflux and aspiration.

Azo Compounds↗

Antisense oligodeoxynucleotide to a delta-opioid receptor selectively blocks the spinal antinociception induced by delta-, but not mu- or kappa-opioid receptor agonists in the mouse.

An antisense oligodeoxynucleotide (A-oligo) to delta-opioid receptor mRNA was utilized to block the expression of mouse delta-opioid receptor in the spinal cord of male ICR mice. Intrathecal treatment with A-oligo (1.6-163 pmol) dose-dependently attenuated the antinociception induced by i.t. administered DPDPE ([D-Pen2,5]enkephalin) or [D-Ala2]deltorphin II, delta-opioid receptor agonist, without affecting the antinociception induced by DAMGO ([D-Ala2-MePhe4,Gly(ol)5]enkephalin) or U50,488H, respective mu- or kappa-opioid receptor agonists. Scrambled sense oligodeoxynucleotide (163 pmol) was ineffective against the tail-flick inhibition induced by DPDPE,[D-Ala2]deltorphin, DAMGO or U50,488H. The studies confirm previous pharmacological studies at the molecular level indicating a distinct delta-opioid receptor for antinociception in the spinal cord.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

Deletion map of the coloboma (Cm) locus on mouse chromosome 2.

The extent of the semidominant coloboma (Cm) mutation on mouse Chromosome 2 was determined by deletion mapping using interspecific hybrid mice. The Cm deletion mutation results in ophthalmic dysmorphology and behavioral deficits, including profound hyperactivity, and has been shown to encompass the gene Snap. In addition to Snap, the gene encoding phospholipase C beta-1 (Plcb-1), which maps 0.60 +/- 0.60 cM proximal to Snap, and simple sequence repeat (SSR) loci D2Mit19, D2Mit46, D2Mit28, and D2Mit136 were shown to be deleted at the Cm locus. In contrast, analysis of other closely linked SSRs and genes either proximal (Bmp-2a) or distal (Nec-1) to Snap, as well as a complementation test with the closely linked mutation lethal milk (lm), indicates that these gene sequences are unaffected by the Cm mutation. These data demonstrate that the Cm deletion represents a contiguous gene defect encompassing 1.1 to 2.2 cM that may be probed for genes, both in the mouse and in the syntenic region of human Chr 20, that independently affect elements of neurological behavior and eye development.

Animals↗

Antisense oligodeoxynucleotide to a delta-opioid receptor given intrathecally blocks i.c.v. administered beta-endorphin-induced antinociception in the mouse.

The antinociception induced by supraspinally administered beta-endorphin is mediated by the release of Met-enkephalin and subsequent stimulation of delta-opioid receptors from the spinal cord in mice. Repeated intrathecal administration of an antisense oligodeoxynucleotide against delta-opioid receptors selectively attenuated i.c.v. administered beta-endorphin-induced antinociception without any effect on the antinociception induced by mu-opioid receptor agonists, morphine and DAMGO, or kappa-opioid receptor agonists, U50,488H. A random sequence oligodeoxynucleotide was inactive against beta-endorphin-induced antinociception. The study confirms previous findings that the antinociception induced by beta-endorphin is mediated by the stimulation of the delta-opioid receptors in the spinal cord.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

An unusual case of maternal-fetal death due to vaginal insufflation of cocaine.

Air embolism secondary to vaginal insufflation has been documented as a cause of death in pregnant women. Under pressure, the air enters the uterus, causing air emboli within the uterine venous drainage and subsequently the systemic circulation. Death is usually sudden as the air obstructs the normal flow of circulation. Acute cocaine toxicity is also a well-known cause of sudden death. Cocaine use is prevalent in our society, even among pregnant women. We report the sudden death of a 31-year-old gravid female and 39-week gestational age male fetus. The cause of death was air embolism secondary to oral-vaginal insufflation of cocaine smoke.

Administration, Intravaginal↗

Case report: fatal Staphylococcus aureus sepsis from single-donor platelet transfusion.

Bacterial sepsis is a rare and potentially fatal complication of platelet transfusions. Bacterial contamination is estimated to occur in 2% to 6% of platelet concentrates, but clinically apparent septicemia occurs in less than 1% of multi-donor platelet transfusions. The incidence of bacterial sepsis from single-donor platelet transfusions is significantly lower, possibly because of shorter storage time of apheresis platelets. The authors report a case of fatal Staphylococcus aureus sepsis from a single-donor platelet transfusion obtained through a closed system. They conclude that as the demand for platelet transfusion increases, recognition of bacterial sepsis from transfusions and continued reassessment of procedures for collection and storage of platelet concentrates is warranted.

Aged↗

Identification of sperm and non-sperm male cells in cervicovaginal smears using fluorescence in situ hybridization: applications in alleged sexual assault cases.

The identification of spermatozoa or constituents of seminal fluid is critical in the evaluation of alleged sexual assault victims. However, failure to identify sperm and/or elevated levels of acid phosphatase can occur for a variety of reasons. Molecular techniques, such as molecular cytogenetic analysis offers new approaches to improve on the identification of male cells in alleged sexual assault cases. Fluorescence in situ hybridization (FISH) with a Y chromosome specific DNA probe was applied to archival cervicovaginal smears from 41 alleged sexual assault cases to identify Y-bearing (male) cells. FISH identified Y-bearing sperm and non-sperm cells in 78% of the cases previously confirmed to have sperm. FISH also identified Y-bearing non-sperm male cells in 39% of the cases in which cytology did not detect spermatozoa; in one of these instances, it also detected sperm. Cervicovaginal acid phosphatase levels, determined at the time of the cervicovaginal smears, were also compared with the presence or absence of Y-positive cells. Application of this technique can detect non-spermatozoic male cells in routine cervicovaginal smears of sexual assault victims.

Acid Phosphatase↗

A retrospective and prospective study of cerebral tissue pulmonary embolism in severe head trauma.

In an attempt to determine the incidence of pulmonary embolization of cerebral tissue as the result of severe head trauma with and without dural penetration, we have collected the autopsy reports at our institution of all head injury victims over the past 3.5 years. The retrospective and prospective histologic examination of these cases revealed a total of 10% to have emboli of cerebral tissue within the pulmonary vasculature. Immunohistochemical staining of the emboli confirmed the neural origin of the tissue. The dura mater proved to be intact in 70% of the cases of cerebral embolization. We feel this provides evidence that embolization of cerebral tissue may occur without rupture of the dura and/or large venous sinuses. This observation is of clinical as well as forensic importance, as cerebral tissue emboli are a rich source of thromboplastin in the systemic and pulmonary vasculature and may contribute to the morbidity and mortality of head injuries.

Adolescent↗

Interpretation of fatal, multiple, and exiting gunshot wounds by trauma specialists.

Firearm-related injuries are a leading cause of morbidity and mortality in the United States. Trauma care centers and trauma specialists (emergency medicine, trauma surgery, and neurosurgery) provide emergency care for those injured and mortally wounded from firearms. Consequently, trauma specialists may be asked to address forensic questions regarding gunshot wounds. Many firearm-related injuries are nonfatal and ultimately, fatal gunshot wounds can suffer from surgical alteration or, if the time interval between injury and death is prolonged, considerable healing of entrance and exit wounds may occur. Thus, accurate initial evaluation of firearm-related injuries is essential. We reviewed all firearm-related fatalities at our institution over the last five and a half years. Our objective was to determine how accurately trauma specialists can differentiate entrance and exit wounds in fatal perforating (exiting) gunshot wounds and determine the number of penetrating or perforating projectiles in fatal multiple gunshot wounds. A total of 271 fatal gunshot wound deaths were reviewed. Of these, we excluded all fatal penetrating (nonexiting) single gunshot wounds and fatalities not evaluated by trauma specialists. Postmortem findings were compared with the medical records from those individuals seen in the emergency department and/or admitted to North Carolina Baptist Hospital (Level I trauma center). Forty six cases with fatal multiple or exiting gunshot wounds were identified. Twenty four (52.2%) were misinterpreted by trauma specialists. Errors included inaccurate determination of the total number of multiple penetrating and/or perforating gunshot wounds and erroneous identification of entrance and exit wounds. Of the exiting, single gunshot wounds 37% were misclassified and 73.6% of multiple gunshot wounds were interpreted incorrectly.(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnostic Errors↗

Partial antinociceptive cross-tolerance to intracerebroventricular beta-endorphin in mice tolerant to systemic morphine.

The effects of subcutaneous morphine pellet-implantation on antinociception induced by intracerebroventricular (i.c.v.) administration of beta-endorphin or morphine and intrathecal (i.t.) administration of morphine, [D-Pen2,D-Pen5]enkephalin (DPDPE), [D-Ala2,NMePhe4,Gly5-ol]enkephalin (DAMGO), serotonin or norepinephrine were studied in male ICR mice. The tail-flick and hot-plate responses were used for antinociceptive tests. The ED50 values for i.c.v. administered morphine for antinociception in morphine pellet-implanted mice were increased from 3.3- and 2.2-fold at 0 h to 14.2- and 19.0-fold at 4 h and declined to 4.8- and 3.0-fold at 8 h after pellet removal in the tail-flick and hot-plate tests, respectively. On the other hand, the ED50 values for i.c.v. administered beta-endorphin for antinociception were only slightly increased (1.7- to 5.1-fold increases) throughout the same time course. The inhibition of the tail-flick response induced by i.t. injection of morphine, DPDPE and serotonin, but not norepinephrine or DAMGO, was attenuated in morphine pellet-implanted mice. These findings are consistent with previous studies indicating that different neuronal mechanisms are involved in morphine- and beta-endorphin-induced antinociception.

Analgesics↗

Spinal delta 2 but not delta 1 opioid receptors are involved in intracerebroventricular beta-endorphin-induced antinociception in the mouse.

The antinociception induced by beta-endorphin given intracerebroventricularly (i.c.v.) has been previously demonstrated to be mediated by the release of Met-enkephalin and subsequent stimulation of delta receptors in the spinal cord for antinociception. The present study was designed to determine what type of opioid receptor, delta 1 or delta 2, in the spinal cord is involved in i.c.v. beta-endorphin-induced antinociception. Antinociception was assessed by the tail-flick test in male ICR mice. NTB (0.2-20 nmol) and NTI (0.22-2.2 nmol), selective delta 2 receptor antagonists, given intrathecally (i.t.) dose-dependently attenuated i.c.v. beta-endorphin-induced inhibition of the tail-flick response. On the other hand, BNTX (0.02-2.2 nmol), a selective delta 1 receptor antagonist, given i.t., did not block i.c.v. beta-endorphin-induced antinociception. The tail-flick inhibition induced by DAMGO, a mu receptor agonist, or U50,488H, a kappa receptor agonist, was not blocked by i.t. BNTX, NTB or NTI. It is concluded that delta 2 but not delta 1 receptors in the spinal cord are involved in i.c.v. beta-endorphin-induced antinociception.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

Spinal involvement of both dynorphin A and Met-enkephalin in the antinociception induced by intracerebroventricularly administered bremazocine but not morphine in the mouse.

Previous reports show the tail-flick inhibition induced by bremazocine given i.c.v. is mediated by supraspinal stimulation of both epsilon and kappa opioid receptors and the spinal activation of descending serotonergic and opioid systems. The present studies questioned what endogenous opioid peptides in the spinal cord were involved in i.c.v. bremazocine-induced antinociception in male ICR mice. beta-Endorphin, trans(+-)-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)cyclohexyl]- benzene-acetamide methane sulfonate (U50,488H) and morphine were used as reference compounds for epsilon, kappa and mu opioid receptor activity, respectively. Intrathecal pretreatment with antibody to Met-enkephalin dose-dependently attenuated the antinociception induced by i.c.v. bremazocine or beta-endorphin but not morphine or U50,488H; whereas intrathecal (i.t.) pretreatment with antibody to dynorphin A (1-13) dose-dependently blocked the antinociception induced by i.c.v. bremazocine or U50,488H but not beta-endorphin or morphine. Intrathecal Leu-enkephalin and beta-endorphin antibodies did not block i.c.v. bremazocine, beta-endorphin or morphine antinociception. Intrathecal Met-enkephalin or dynorphin A (1-17) increased the tail-flick latency at 1 to 2 min. Met-enkephalin given i.t. blocked the antinociception induced by i.c.v. DPDPE, bremazocine and beta-endorphin but not morphine or U50,488H whereas i.t. dynorphin A (1-17) pretreatment blocked the inhibition induced by i.c.v. U50,488H and bremazocine but not DPDPE, beta-endorphin or morphine. Bremazocine given i.c.v. did not exhibit antianalgesic activity in our studies. The dynorphin released by i.c.v. bremazocine for antinociception appears to be different from the dynorphin released by morphine for antianalgesia.(ABSTRACT TRUNCATED AT 250 WORDS)

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

The tail-flick inhibition induced by beta-endorphin administered intrathecally is mediated by activation of kappa- and mu-opioid receptors in the mouse.

The inhibition of the tail-flick response induced by beta-endorphin given i.c.v. has been demonstrated to be mediated by the stimulation of epsilon- but not mu-, delta- or kappa-opioid receptors. beta-Endorphin given i.t. also inhibited the tail-flick response. The present studies were designed to determine what types of opioid receptors in the spinal cord were involved in i.t. beta-endorphin-induced tail-flick inhibition. Blockade of kappa-opioid receptors by coadministration of nor-binaltorphimine or Win 44,441-3 with beta-endorphin given i.t. dose dependently inhibited i.t. beta-endorphin-induced inhibition of the tail-flick response. Blockade of mu-opioid receptors by i.t. coadministration of D-Phe-Cys-Tyr-D-Try-Orn-Thr-Pen-Thr-NH2 with beta-endorphin blocked i.t. beta-endorphin-induced inhibition of the tail-flick response. I.t. injection of delta-opioid receptors antagonists, ICI 174,864 and naltrindole, or epsilon-opioid receptor antagonist, beta-endorphin-(1-27), did not affect inhibition of the tail-flick response induced by beta-endorphin given i.t. Blockade of alpha 2-adrenoceptors and 5-HT receptors by i.t. injection of yohimbine and methysergide, respectively, also did not affect inhibition of the tail-flick response induced by beta-endorphin given i.t. The results indicate that the inhibition of the tail-flick response induced by beta-endorphin given i.t. is mediated by the stimulation of kappa- and mu-opioid receptors but not delta- and epsilon-opioid receptors, alpha 2-adrenoceptors or 5-HT receptors.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗