Biomedical subjects
Publications and source records attributed to C Kaur.
Laugier-Hunziker syndrome is a benign pigmentary disorder which manifests as macular hyperpigmentation of the lips and buccal mucosa. Some patients have longitudinal pigmented bands of nails. The syndrome has no systemic associations. Two patients of this rare syndrome are reported. Disorders producing similar pigmentary changes which must be differentiated are discussed.
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This study examined the effects of high altitude exposure on neurons in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus in adult and neonatal rats. In adult control rats, occasional Fos-like immunoreactive neurons were localized in both the hypothalamic nuclei. A marked increase in Fos positive cells was induced at 1-4 h following altitude exposure but it was reduced to levels comparable to the controls at 24 h. The expression of neuronal nitric oxide synthase (nNOS) immunoreactivity in the PVN and SON followed a similar temporal pattern. The nNOS immunoreactivity, which was constitutively expressed in the hypothalamic neurons in the control rats, was noticeably augmented at 1-4 h, but it was comparable to the controls at 24 h following altitude exposure. In postnatal rats, Fos expression was not detected in the hypothalamic neurons of the controls. Induction of Fos expression was observed in some neurons at 1-4 h following altitude exposure but it was diminished at 24 h. There was no noticeable change in nNOS expression in both the control and altitude exposed postnatal rats; in both instances, it was barely detectable. It is concluded that both the PVN and SON of the adult rats are activated at high altitude exposure and that they may be involved in the regulation of neuroendocrine, cardiovascular and respiratory functions in hypobaric hypoxia. This study has also shown the differential response of the hypothalamus neurons between the two age groups to the hypoxic insult. Our results suggest that the adult neurons are probably more sensitive to the reduced oxygen levels in hypobaric hypoxia, as reflected by the upregulated NOS expression in this age group but not in the postnatal rats.
This study aimed to examine the temporal profile of neuronal apoptosis in the central nervous system (CNS) following closed head injury in rat. Fos immunoreactivity was detected in neuronal nuclei in the cerebral cortex at 2 h after head injury. At 4 h, Bax protein expression was elevated with a concomitant down-regulation of Bcl-2 expression. Along with this, a marked immunoexpression of p53 was also observed in these cells. Double immunolabelling study has shown the colocalization of Bax immunoreactivity with Bcl-2 and p53. In rats killed 1 day after injury, a variable number of transferase d-UTP nick-end labelling positive cells were observed. Present findings suggest that the upregulation of p53 and a shift in the ratio of Bcl-2 to Bax may contribute to neuronal apoptosis in the CNS after closed head injury.
The ameboid microglial cells (AMC), located in the periventricular white matter, were examined ultrastucturally in neonatal rats following a hypoxic exposure. For 10 min to 1 day, following the hypoxic exposure, a large number of glial cells with nuclear chromatin condensation, undergoing degeneration, were observed in the white matter. Such cells were often being phagocytosed by the AMC. At 3-7 days after the hypoxic exposure, the cytoplasm of many AMC contained a number of phagosomes whereas at 14-28 days a large amount of lipid accumulation was observed in them. AMC were labeled intensely with horseradish peroxidase (HRP) administered intraperitoneally following the hypoxic exposure. The phagocytosis of degenerating cells by the AMC and uptake of HRP by them indicates that these cells efficiently remove the degenerating cells/debris from the neonatal white matter following hypoxia in an attempt to protect it from any harmful substances that may be secreted by the degenerating cells or from serum derived substances that may enter the brain through blood circulation.
The present study examined effects of high altitude exposure, which leads to development of hypoxia, on epiplexus cells associated with the choroid plexus in adult rats. At 2-5 h following exposure, epiplexus cells expressing inducible nitric oxide synthase (iNOS) were commonly observed. Increased expression of complement type 3 receptors (CR3) and major histocompatibility complex class II (MHC II) antigens was also observed 4-14 days after altitude exposure. It is suggested that the early expression of iNOS in epiplexus cells following an altitude exposure may protect the choroid plexus and ventricles from damage caused by reactive oxygen species during reoxygenation. The enhanced expression of CR3 receptors and MHC II antigens at later time intervals may be involved in protection of cerebral ventricular system from any infection that may accompany or follow altitude exposure.
The present study showed the expression of induced nitric oxide synthase (iNOS) immunoreactivity in amoeboid microglia following an exposure to transient hypoxia in postnatal rats. iNOS immunoreactivity was expressed mainly in the amoeboid microglia in corpus callosum and subependymal regions of the ventricles within 3 h after hypoxia. The expression declined after 5 h, and became undetectable after 15 h and in longer surviving rats. The immunoreactivity of these cells with OX-42, which is a marker for microglia cells and detects complement type three receptors (CR3), was comparable in the rats exposed to hypoxia and the control rats. Immunoglobulin G (IgG) immunoreactivity was observed in the amoeboid microglia up to 3 h after hypoxia but it was undetectable in longer surviving rats and in the control rats. The iNOS expression in the amoeboid mircoglial cells may be related to the host defense and maintenance of structural integrity of the highly vulnerable periventricular white matter after hypoxia. The immunostaining of amoeboid microglial cells with IgG following hypoxia indicates leakage of plasma immunoglobulin from the blood vessels and its removal by the amoeboid microglial cells.
This study was aimed to ascertain the effects of hypoxia on regulation of iron in the brain of newborn rats. At 3 h and 1 day after hypoxic exposure transferrin receptor expression as detected immunohistochemically with the antibody OX-26, and the iron content as shown by Perls' staining of amoeboid microglial cells was markedly increased. The induced changes, however, were not evident at 10 min and in longer surviving rats killed at 3 and 7 days. It is suggested that the upregulation of transferrin receptor expression coupled with iron uptake by amoeboid microglial cells in the periventricular regions is a protective mechanism to facilitate the sequestration of excess iron that may have been released either from the iron-rich oligodendrocytes, or accumulated due to a disruption of its normal transportation following the hypoxic insult. This would help protect the brain from harmful effects of iron.
The present study examined the response of macrophages/microglia to multiple injections of melatonin in the pineal gland and different regions of the brain. The macrophages/microglia showed a significant increase in cell numbers and upregulation of complement type 3 receptors (CR3), major histocompatibility complex class I (MHC I) and class II (MHC II) antigens, and antigens of monocyte/macrophage lineage, as detected by the antibodies OX-42, OX-18, OX-6, and ED1, respectively. The upregulation of the above antigens was observed in 1-d-old rats given daily injections of melatonin and killed at 7-11 d of age; no noticeable change was observed at earlier time intervals. The macrophages/microglia expressing the above antigens appeared round and showed a vacuolated cytoplasm compared with ramified cells in the control rats. Upregulation of CD4 antigens as detected with the antibody W3/25 was also observed in macrophages/microglia in the corpus callosum and epiplexus cells in the lateral ventricles, but not in the pineal gland and the cerebral cortex in the same age group. In rats killed between 2 and 5 d, and at 14 d of age after melatonin treatment, the immunoreactivities of macrophages/microglia with the above mentioned antibodies were comparable to cells in the control rats. Immunoreactive cells were not detected in any of the age groups in melatonin-treated or control rats with the antibodies W3/13 and OX-33, which are markers for T and B lymphocytes. It is concluded that CR3 receptors, MHC antigens, and CD4 antigens on macrophages/microglia are upregulated following melatonin administration. On the other hand, once the melatonin treatment is discontinued the expression of the various antigens/receptors returns to normal levels, suggesting that increased immune potentiality and its maintenance in these cells require the continuous action of the drug.
The present study has demonstrated the induction of nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) reactivity and nitric oxide synthase-like immunoreactivity (NOS-LI) in the ventral horn motoneurons of the spinal cord in rats subjected to a single or multiple underground, or a single surface blast. Both enzyme activities were first detected in some motoneurons in laminae VIII and IX of Rexed, 3 hours after the blast. Some NADPH-d and NOS-LI positive neurons were also distributed in laminae VI and VII. The number and intensity of the labelled cells appeared to increase progressively, peaking at 2-3 days after the blast but were drastically reduced thereafter, so that at 7 days after the blast only a few positive neurons were observed. In rats killed at 2 weeks and in longer surviving intervals, i.e. up to 1 month, NADPH-d/NOS reactivity in the ventral horn motor neurons had diminished. The functional significance of the transient expression of neuronal NADPH-d/NOS after the blasts remains uncertain, although from a speculative point of view, the induction of these enzymes probably would reflect an increased production of nitric oxide (NO). In view of the lack of atrophic changes in most, if not all, of motor neurons, it is suggested that the increased levels of NO production after the blast injury may be involved in a neuroprotective function.
Intraventricular macrophages encompass the supraependymal, free-floating, and epiplexus (Kolmer) cells; the supraependymal cells lie in close apposition to the ventricular ependyma, the epiplexus cells are closely associated with the choroid plexus epithelium, and the free-floating cells are at a variable distance from the epithelial surface. Although the three cell types are regarded as one cellular entity, the epiplexus cells preponderate. On scanning electron microscopy, the epiplexus cells display diverse morphological forms, ranging from round to bipolar to stellate, and bear a variable number of cytoplasmic processes. Transmission electron microscopy shows the presence of large numbers of lysosomes. The phagocytic nature of epiplexus cells is shown by their intense staining for nonspecific esterase and active uptake of tracers, e.g., horseradish peroxidase and rhodamine isothiocynate, administered intravenously or intraperitoneally. The mode of entry of these tracers in the cerebral ventricles is by way of transepithelial transport. In rats, the population of intraventricular macrophages increases steadily after birth until 17 days of age; thereafter, their cell population remains relatively unchanged. The early upsurge is attributed to proliferation of residential cells and/or influx of circulating monocytes/stromal macrophages through the process of "emperipolesis." The immunophenotypic features of intraventricular macrophages are consistent with other mononuclear phagocytes being immunoreactive for OX-42, OX-18, OX-6, and OX-1 and ED1 for the detection of CR3 receptors, MHC class I and II antigens, leucocyte common antigen, and macrophage antigen, respectively. The expression of these antigens is noticeably enhanced following the injection of lipopolysaccharide (LPS) into postnatal rats. Remarkably, the intraventricular macrophages are induced to express MHC class II (Ia) antigen after LPS or interferon-gamma injections. Furthermore, the expression of transferrin receptors as detected with OX-26 is also upregulated after these treatments. Epiplexus cells are also elicited to display a de novo expression of nitric oxide synthase-like immunoreactivity following intracerebral injection of LPS. They also respond vigorously to a single nonpenetrative blast. Results of our series of studies suggest that, besides their primary function as scavenger cells, the intraventricular macrophages partake in possible immunological responses and iron regulation in the ventricular system or the brain as a whole.
This study examined the neuropathological changes in different areas of the brain of fetal and postnatal rats after transient maternal hypoxia. At different time intervals following hypoxia, reactive microglia as determined immunohistochemically with the antibody OX-42 that recognizes complement type three (CR3) receptors, responded vigorously to the hypoxic stress. Microglial activation was particularly evident in the cingulate cortex and the corpus callosum between 3 h and 14 days after hypoxia. Massive cell degeneration as determined ultrastructurally and significant neuronal loss as evaluated by cell counts were observed in the cingulate cortex at 1 and 3 days after hypoxic insults; thereafter, however, the neuronal density was restored to normal levels. Present results suggest that the cingulate cortex is most vulnerable to the hypoxic injury probably due to a redistribution of cerebral blood flow and/or metabolic changes. Besides being involved in the phagocytosis of cellular debris, it is suggested that the reactive microglial cells may have both neurotoxic and neurotrophic functions.
1-day old postnatal rats were given daily intraperitoneal injections of chloroquine and sacrificed at various time intervals thereafter. In rats killed at 7 and 14 days of age a large number of cytoplasmic lamellar bodies were induced in the pinealocytes. The macrophages/microglia among the pinealocytes showed the presence of large dense bodies in their cytoplasm. In chloroquine injected rats killed at 21 days of age, the lamellar bodies had vanished. The macrophages/microglia were comparable to those in the control animals. Cytoplasmic lamellar bodies were not observed in the pinealocytes of the control rats in any age group and in rats killed at 2 and 4 days of age following chloroquine injections. The pineal macrophages/microglia in these rats showed the presence of only some small dense granules in their cytoplasm. The immunoreactivity of the macrophages/microglia with OX-42, OX-18, OX-6 and ED1 which detect the complement-type 3 receptors, major histocompatibility complex class I and class II antigens and monocyte/macrophage antigens respectively was comparable in chloroquine injected and control rats. The labelling of the macrophages/microglia with rhodamine isothiocyanate (RhIC) in 7 days old chloroquine injected rats was also comparable to the labelling of cells in the corresponding control rats. It is concluded from this study that although repeated chloroquine administration induces acute structural alteration of the pinealocytes and macrophages/microglia in the pineal gland, its effects are reversible since the cells regained their normal ultrastructural features following discontinuation of the drug. The immune functions and phagocytic activity of the macrophages/microglia shown by their immunoreactivity with various antibodies and RhIC labelling respectively are not altered by chloroquine.
Mycoplasma capricolum subsp. capripneumoniae of cow-udder origin was tested in rabbit mammary-glands for its mastitogenic capability. Establishment of mycoplasma organisms and presence of histopathological lesions in mammary glands were the parameters for describing mastitogenic potential. The reisolation of injected Mycoplasma capricolum subsp. capripneumoniae organisms in the pure form from the infected glands along with the occurrence of histopathological changes were suggestive of mastitis during the entire 8-days period of observation. Rabbit mammary-gland is recommended as a potential in vivo experimental laboratory model to screen the mastitogenic potential of mycoplasmas of animal-udder origin.
Amoeboid microglial cells (AMC) in fetal brains were labeled by rhodamine B isothiocyanate (RhIc) when injected intravenously or intraperitoneally into mother rats at late state of pregnancy. The fluorescent cells were immunostained with antibodies OX-42 and OX-18 that recognize complement type 3 (CR3) receptors and major histocompatibility complex class I (MHC-I) surface antigen, respectively. RhIc-labeled AMC were first observed in the cavum septum pellucidum and subependymal cysts associated with the cerebral aqueduct as well as the fourth ventricle, and subsequently at other sites including the corpus callosum and other subcortical white matter. The fluorescence intensity increased with time after RhIc administration so that after 1 day the cells were brightly labeled. The majority of the labeled cells were round, with some elongated ones bearing two or three processes. Besides AMC, macrophages in the ventricular system were also labeled. All fluorescent cells were double labeled with OX-42 and OX-18 antibodies. Present results suggest that when introduced into the maternal circulation, RhIc could readily gain access into the fetal brain through the inefficient placental, blood-brain and blood-cerebrospinal-fluid (blood-CSF) barriers. The avid uptake of RhIc in circulation by brain macrophages indicates an active scavenging role of these cells in fetal brain. The labeling of cells by maternal route offers a rapid method for study of distribution of brain macrophages in fetuses.
The pineal gland of adult rats was examined immunohistochemically and electron microscopically following exposure of the animals to a single blast equivalent to 110 kg TNT explosive. The most dramatic feature in rats killed at 7, 14 and 21 days after the blast was the upsurge of a large number of macrophages/microglia intensely immunostained with OX-42, OX-18, OX-6 and ED1 antibodies. These antibodies recognise the complement type three (CR3) receptors, major histocompatibility complex class I and class II (MHC I and MHC II) antigens and monocyte/macrophage antigens. Cell counts in OX-42 immunostained sections showed a two-fold increase at these intervals but returned to normal values at 28 days. The immunolabelled cells appeared extremely hypertrophic after the blast when compared with those in normal rats. In the latter and in rats killed at 28 days after the blast, immunoreactive cells were sparsely distributed. Ultrastructural study confirmed a wider occurrence of perivascular macrophages/microglia after the blast and the cells were laden with massive amounts of phagosomes resembling degenerating pinealocyte processes. It is concluded that the seemingly quiescent macrophages/microglia present normally in pineal gland were activated by the external blast force. The induced changes including the increase in cell numbers and endocytosis, however, were reversible in longer surviving animals.
The pineal gland of rats of various ages (1-21 days old) was examined by immunohistochemistry and electron microscopy. Numerous widely distributed cells identified as macrophages/microglia were immunoreactive with the monoclonal antibodies OX-42, OX-18, OX-6, and ED1, indicating that they expressed complement type 3 (CR3) receptors, major histocompatibility complex class I and II antigens, and antigens of monocyte/macrophage lineage as detected by the antibodies, respectively. Following an intraperitoneal injection of rhodamine isothiocyanate (RhIC) in all age groups, the cells emitted a bright fluorescence. They were also labeled by horseradish peroxidase (HRP), as demonstrated in both light and electron microscopy. An HRP reaction was observed in vesicles and lysosomes at the ultrastructural level. A remarkable feature was the uptake of these tracers by pinealocytes. In light microscopy, the pinealocytes showed a punctate reaction product 3-24 hours after HRP injection. By electron microscopy, the reaction product was observed in vesicles, lysosomes, and some rod-like structures in the cytoplasm. On the basis of their immunophenotypic features, it is suggested that the macrophages/microglia in the pineal gland are active phagocytes which are also probably involved in the immunoregulatory function in the gland. The avid uptake of RhIC and HRP from the circulation by these cells suggests that serum-derived substances that may gain access to the parenchyma of the gland are being constantly monitored. The labeling of pinealocytes with HRP suggests that the functional activities of these cells are being modulated by serum-derived substances.
The present study was conducted to examine the response of amoeboid microglial cells in the postnatal rat brain to colchicine administration. One-day-old postnatal rats were given intraperitoneal injections of colchicine and sacrificed at 7, 14 and 21 days of age. In rats killed at 7 days age, the number of OX-42, OX-18 and ED1 positive amoeboid microglial cells was considerably reduced when compared with the control rats. At 14 and 21 days, the number of cells immunoreactive with the above antibodies was comparable to that of the control rats. The intensity of the immunoreaction with the various antibodies was also comparable in colchicine injected and control rats. When rhodamine isothiocyanate (RhIC) was administered, amoeboid microglial cells emitted a bright fluorescence in control rats as well as in colchicine-injected rats, although in the latter, the number of RhIC labelled cells was considerably reduced. With the antibody bromodeoxyuridine a large number of stained cells were observed in the control rats. On the other hand, occasional labelled cells were recognized in colchicine-injected rats. Apoptotic amoeboid microglial cells were observed in 4-day-old colchicine-injected rats. At the electron microscopic level, amoeboid microglial cells in colchicine-injected rats killed at 7 days of age showed a large number of phagosomes in their cytoplasm compared with the corresponding control rats. At 14 and 21 days, in colchicine-injected and control rats, amoeboid microglial cells did not display any noticeable differences. It is concluded from the present study that colchicine suppresses the number of amoeboid microglial cells, and that this may be attributed to the antimitotic effect of the drug as well as apoptosis induced by it; the phagocytic activity, however, was not affected. The cells returned to their normal population and morphological features once the drug was discontinued, indicating the reversible nature of the drug effect.