Physicochemical and sensory properties of ice-cream formulated with virgin coconut oil.

The substitution of milk fat with virgin coconut oil (VCO) was used to produce nutritious ice cream with pleasant coconut flavor and aroma. Three formulations were developed whereby formulation VCO4, VCO8 and VCO12 was substituted with 4%, 8% and 12% of VCO, respectively. The physicochemical properties of ice creams analyzed include overrun, meltdown, pH, titratable acidity, total solid, protein and fat content. The fatty acids profile of VCO formulated ice creams and their stabilities over 3 and 6 weeks storage were studied respectively using gas chromatography (GC). Qualitative descriptive analysis (QDA) and consumer affective test were performed among the trained and untrained panelists. Significant differences (p < 0.05) of overrun, pH, total solid, protein and fat content between ice cream formulations were observed except titratable acidity. Increased VCO content in ice cream formulations lowered the melting resistance of ice cream. For GC analysis, the major fatty acid identified was lauric acid. Upon storage time, the concentration of unsaturated fatty acid decreased but the concentration of saturated fatty acid increased. The result of QDA showed that formulation VCO4, VCO8 and VCO12 were significantly (p < 0.05) different in attributes of color, firmness and smoothness as compared to the control ice cream. Formulation VCO12 was highly accepted by panelists in terms of the acceptance level of appearance, aroma, texture, flavor and overall acceptability. Hence, it has a potential marketable value.

Dopaminergic cell death precedes iron elevation in MPTP-injected monkeys.

Though increasing lines of evidence suggest that iron accumulation and iron-induced oxidative stress might be important pathological factors responsible for substantia nigra (SN) cell death in Parkinson's disease (PD), it is still unknown whether iron accumulation is a primary cause or consequence of nigral cell death. Using nuclear microscopy, iron histochemistry, TUNEL method for apoptosis detection, and tyrosine hydroxylase (TH) immunohistochemistry, the present study investigated possible changes in iron contents in the SN and correlations of dopaminergic cell death progression with the process of iron accumulation in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced parkinsonian monkey from 1 d to 18 months after MPTP administration. Our study demonstrated that apoptosis occurred in the ipsilateral SN at 1 d after MPTP injection and the number of TH-positive cells decreased significantly from 1 week onward. However, iron content was significantly increased in the ipsilateral SN from 4.5 months to 18 months after MPTP injection, and the iron increase was significantly correlated to the extent of dopaminergic cell death. These results suggest that dopaminergic cell death induced by MPTP administration might lead to iron accumulation in the monkey SN, and increased iron might contribute to the progression of nigral degeneration.

Data mining applications in the context of casemix.

In October 1999, the Singapore Government introduced casemix-based funding to public hospitals. The casemix approach to health care funding is expected to yield significant benefits, including equity and rationality in financing health care, the use of comparative casemix data for quality improvement activities, and the provision of information that enables hospitals to understand their cost behaviour and reinforces the drive for more cost-efficient services. However, there is some concern about the "quicker and sicker" syndrome (that is, the rapid discharge of patients with little regard for the quality of outcome). As it is likely that consequences of premature discharges will be reflected in the readmission data, an analysis of possible systematic patterns in readmission data can provide useful insight into the "quicker and sicker" syndrome. This paper explores potential data mining applications in the context of casemix by using readmission data as an illustration. In particular, it illustrates how data mining can be used to better understand readmission data and to detect systematic patterns, if any. From a technical perspective, data mining (which is capable of analysing complex non-linear and interaction relationships) supplements and complements traditional statistical methods in data analysis. From an applications perspective, data mining provides the technology and methodology to analyse mass volume of data to detect hidden patterns in data. Using readmission data as an illustrative data mining application, this paper explores potential data mining applications in the general casemix context.

Qualitative light and electron microscope study of glutamate receptors in the caudal spinal trigeminal nucleus of the rat.

Though ionotropic and metabotropic glutamate receptors have recently been recognized to play important roles in the transmission of orofacial nociceptive impulses, their detailed distribution in the spinal trigeminal nucleus has not been systematically investigated. There is also controversy regarding the electron microscope localization of metabotropic receptors. We therefore undertook this investigation to address the above-mentioned issues in the caudal part of the spinal trigeminal nucleus, using light and electron microscope immunocytochemistry, to provide baseline information for the development of agonists and antagonists of these receptors in the clinical treatment of orofacial pain. The results showed some moderately to strongly stained glutamate receptor 1 neurons, and many strongly stained glutamate receptor 2/3 neurons in lamina II of the nucleus, suggesting that the latter may play an important role in orofacial pain processing, with the former playing a minor role. The metabotropic glutamate receptor 1 immunoreactive product was localized mostly in dendrites, while most of the metabotropic glutamate receptors 2/3 immunoreactive product was deposited in axon terminals containing synaptic vesicles of different shapes, suggesting that glutamate receptors 2/3 may control the release of both excitatory and inhibitory neurotransmitters.

Sustained microglial immunoreactivity in the caudal spinal trigeminal nucleus after formalin injection.

Recent studies indicate that glia may be involved in altered nociceptive processing after a peripheral inflammatory lesion produced by injection of inflammatory reagents such as formalin and zymosan. Most of these studies, however, confined their observations to a period shortly after the injections. This study investigated the immunohistochemical responses of microglia in the caudal part of the spinal trigeminal nucleus for up to 60 days after subcutaneous injection of formalin into the lateral faces of Wistar rats. The results showed obvious up-regulation of microglial markers such as OX-18, OX-42 and OX-6 up to 21 days after formalin injection. These were somewhat reduced at 30 days after injection. Electron microscope investigation revealed no evidence of significant phagocytosis of degenerative neuronal elements by microglia in the nucleus at the time--that is, 7 days after formalin injection, when microglial activation was at its peak. Significantly, however, the period of microglial activation corresponded closely to that showing enhanced nociceptive behavior after perioral formalin injection (Cadet et al., 1995). This study indicates a microglial role in the genesis of enhanced nociceptive behavior.

Effects of nitric oxide on normal and ischemic cochlea of the guinea pig.

To determine whether nitric oxide (NO)/peroxynitrite plays any role in neurodestruction observed in ischemic cochlea of the guinea pig, the effects of NO donors like S-nitrosocysteine (S-NC) and nitroglycerin (NTG), peroxynitrite generators like 3-morpholinosydnonimine (SIN-1), peroxynitrite inhibitors like superoxide dismutase plus catalase (SOD/Cat), as well as NOS inhibitors like N(G)-nitro-l-arginine methyl ether (L-NAME), were tested on normal and ischemic cochleae. Various concentrations of S-NC and SIN-1 were introduced into the perilymphatic space of normal guinea pig cochlea. Quantitative scanning electron microscopy of inner and outer hair cells was carried out 2 days later. To determine the level of NO in the cochlea after 20 to 120 min of ischemia, nitrites/nitrates in the perilymph were measured. The effects of NO on the ischemic cochlea were tested by infusion of SOD/Cat, L-NAME, S-NC, and NTG into the perilymphatic space just before decapitation. Introduction of fixative into the cochlea was delayed for 15 min to investigate the effects of the chemicals on nerve endings at the base of inner hair cells. The results showed that the level of nitrites/nitrates tended to decline with increasing time of ischemia. There was no significant hair cell loss in the cochleae treated with SIN-1 or S-NC. At 15 min after ischemia, most of the nerve endings at the base of the inner hair cells were protected from damage when 1 mM S-NC or NTG was infused into the perilymph. Taken together, the results indicate that NO/peroxynitrite is unlikely to be involved in the neurodestruction in the ischemic cochlea. In fact, exogenous NO may have a neural protective effect.

Distinct subcellular localization and mRNA expression of neuronal nitric oxide synthase in the nucleus dorsalis and red nucleus and their correlation with inducible transcription factors after spinal cord hemisection.

We previously reported on the differential expression of neuronal nitric oxide synthase (nNOS) in neurons of the nucleus dorsalis (ND) and red nucleus (RN), as well as differential roles of nitric oxide (NO) in these two distinct groups' neurons characterized with different nNOS phenotypes after lower thoracic spinal cord hemisection. To further understand the enzyme, nNOS expression was studied at the subcellular and mRNA levels by using electron microscopic immunohistochemistry (EM-IHC) and in situ hybridization respectively. Possible transcriptional regulation by c-Jun or CREB in the differential nNOS expression in both ND and RN neurons was also studied. nNOS mRNA was not found in the normal ND neurons, but was shown in the normal RN neurons. After spinal cord hemisection, nNOS mRNA was induced in the ipsilateral ND, while upregulated on both sides of the RN, which preceded protein induction or upregulation. By EM-IHC, nNOS immunoreaction products were predominantly bound to the membrane of the mitochondria, rough endoplasmic reticulum (rER), Golgi apparatus, and nuclear envelope in the RN neurons of normal rats as well as rats subjected to spinal cord hemisection. In contrast, nNOS-immunoreactive deposits in the experimental ND neurons were found to be mainly granular, being dispersed throughout the cytoplasmic matrix. It is speculated that the differential subcellular localizationof nNOS indicates that axotomy may trigger different nNOS transcripts and lead to different nNOS isoform expression in the normally non-nNOS- and normally nNOS-containing neurons. c-Jun was induced in the ipsilateral ND neuronsand upregulated only in the contralateral RN neurons. Activation of CREB by phosphorylation was occasionally detectable in the ND neurons, but not in the RN neurons. Double-labeling data showed a large proportion of c-Jun and nNOS colocalization in neurons of the ipsilateral ND and contralateral RN after spinal cord hemisection. However, dissociation of nNOS expression kinetics with c-Jun was observed in the ipsilateral RN. The results implied that nNOS expression might not be under the direct transcriptional regulation by c-Jun, although it seemed to be closely related to the c-Jun expression.

6-Hydroxydopamine induced apoptosis of dopaminergic cells in the rat substantia nigra.

The pathologic hallmark of Parkinson's disease is the dopaminergic cell death in the substantia nigra (SN). The cause of the cell death is, however, unknown. Even the question on whether the cells die by apoptosis or necrosis has not been answered with certainty. In 6-Hydroxydopamine induced Parkinsonian rats, the present study observed apoptotic nuclei from 1 day to 14 days after lesioning, using the TdT(terminal deoxynucleotidyl transferase)-mediated dUTP-biotin nick-end labeling method. Tyrosine hydroxylase immunohistochemistry and haematoxylin staining further revealed that these apoptotic cells are dopaminergic cells in the substantia nigra. The results suggest that dopaminergic cells in SN undergo apoptosis in the rat model of Parkinson's disease.

Neuroprotective and neurodestructive functions of nitric oxide after spinal cord hemisection.

Nitric oxide (NO) may subserve different functions in different central neurons subjected to axotomy. The difference may depend on whether the neurons basally express neuronal nitric oxide synthase (nNOS), a biosynthetic enzyme of NO. This is supported by our previous finding that suggests the differential role of NO in neurons of nucleus dorsalis (ND) and red nucleus (RN) which have different basal expression of nNOS. This study aimed to establish firmly the functions of NO, as revealed by nNOS immunoreactivity and nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) histochemistry, by the administration of endogenous NO donor, l-arginine (l-arg), and NOS inhibitor, l-N(G)-nitroarginine methyl ester (l-NAME). To relate the role of NO to glutamate receptors (GluR), the distributions of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) and N-methyl-d-aspartate receptor (NMDAR) in the two nuclei were revealed by immunohistochemical techniques. nNOS immunoreactivity was void in ND neurons, but expressed weakly in the RN normally. It was induced in ipsilateral ND neurons and upregulated on both sides of RN after spinal cord hemisection. Neuronal loss in the ipsilateral ND was augmented by l-arg, but reduced by l-NAME. In the contralateral RN, l-arg attenuated neuronal loss. NMDAR1 was present in most neurons in ND. After axotomy, some NMDAR1 immunoreactive neurons of the ipsilateral ND were induced to express NOS, whereas RN neurons showed strong staining for NMDAR1 and all the AMPA subunits. Most of the NOS-positive neurons in the RN were coexistent with GluR2 in normal rats and those subjected to axotomy. The present data demonstrated that NO exerted neurodestructive function in the non-NOS-containing ND neurons characterized by NMDAR as the predominant glutamate receptor. NO might be beneficial to the NOS-containing RN neurons. This could be attributed to the presence of GluR2. Possible diverse synthesizing pathways of NO in two different central nuclei were suggested from the observation that NOS was colocalized with NADPH-d in ND neurons, but not in RN neurons.

Back to basics.

The present study sought to establish findings and share views concerning the teaching of gross anatomy. The conclusions were drawn from feedback taken in 1995 from Year 1 (M1) through Year 5 (M5) (final year) medical students at the National University of Singapore. The survey was taken from two groups of students that had gone through two different curricula. The first group of M4 and M5 students studied under an old curriculum that taught anatomy over a period of three semesters. The second group of M1 through M3 students studied under a new curriculum of two semesters' duration. Altogether, 546 (M1: 147; M2: 120; M3: 78; M4: 107; M5: 97) completed questionnaires were analyzed. Throughout the years of study, the majority of students found dissection helpful (55.2-72. 7%) or very helpful (18.9-40.7%) in their understanding of gross anatomy. A minority of students (0-25.3%) found it not helpful. Taking all of the five years of students together, this would mean that 60.7% of the students found dissection helpful and 28% of them found it very helpful in their understanding of gross anatomy. Of the M3 students who had both dissection and demonstrations on prosected specimens, the majority of them found dissection helpful (55.2%) or very helpful (33.3%); they also found demonstrations on prosected specimens helpful (64.6%), or very helpful (27.8%). When asked whether dissection should be replaced completely by demonstrations on prosected specimens, 86.7% gave a resounding no. With regard to gross anatomy coverage, 11.7% of M4 and M5 students found it inadequate, 67.5% adequate, and 20.8% excessive. Only 1% of these students found that the gross anatomy they had learned was of no clinical relevance; 22.3% found it of little clinical relevance; and an overwhelming majority (76.7%) found it mostly clinically relevant. Most were grateful that they had been taught the basics of gross anatomy. These findings are discussed with an emphasis on the time needed and deep level approach required to gain conceptual understanding of anatomical organization.

Time course of dopaminergic cell death and changes in iron, ferritin and transferrin levels in the rat substantia nigra after 6-hydroxydopamine (6-OHDA) lesioning.

Parkinson's disease is characterized by dopaminergic cell death in the substantia nigra. The underlying mechanism is, however, unknown. Though there are increasing lines of evidence showing iron accumulation in the Parkinsonian substantia nigra, it still remains obscure whether increased iron is the primary cause of dopaminergic cell death, or just a consequence of the pathological process. It is also unclear how iron gains access to the Parkinsonian SN. To gain more understanding in these areas, the present study investigated the time course of dopaminergic cell death and of changes in the level of iron, ferritin and transferrin. The results showed that iron was increased after the significant nigral dopaminergic cell death induced by 6-hydroxydopamine injection into the rat substantia nigra. On the other hand, the expression of transferrin was decreased. However, there was a temporal increase in the number of ferritin positive microglia. The results indicated that iron increase was not the primary cause of dopaminergic cell death in the Parkinsonian rat. It was most likely the result of an accumulation of iron-laden microglia.

Ototoxicity of sodium nitroprusside is not due to nitric oxide.

Sodium nitroprusside (SNP) has been used as a donor for nitric oxide (NO) to study the effects of NO on the mammalian cochlea. In the present study, we set out to determine whether NO was the chemical responsible for the ototoxic effects seen after the application of SNP at the round window membrane of the adult guinea pig cochlea. In the first instance, NO released from S-nitrosocysteine, a compound not related to cyanide, has no toxic effect on the hair cells of the cochlea. Light-exposed SNP that could no longer produce NO, light-exposed SNP to which acetylcysteine (ATC) or hydroxycobalamin (HCL) was added to eliminate cyanide, and freshly prepared SNP to which ATC or HCL was added were also tested. Six groups of animals consisting of three animals in each group were used. The single chemical or combination of chemicals stated above was soaked in a piece of gelfoam that was then applied to the round window membrane of the animal under ketamine-xylasine anesthesia. The animals were reanesthetized 3 days later and perfused for scanning electron microscopy and hair cell quantitative analysis. The results showed that, in animals given S-nitrosocysteine, no hair cell loss was noted, while light-exposed SNP led to severe hair cell damage similar to that seen after the administration of fresh SNP. In animals treated with the mixture of light-exposed SNP and ATC or HCL, or fresh SNP with ATC or HCL, ototoxicity was significantly attenuated. These results have convincingly demonstrated that NO at a certain level is not destructive to auditory hair cells and the hair cell loss observed after SNP application is most likely due to the cyanide released from the SNP instead of NO.

Ultrastructural changes in the chick thymus following unilateral vagotomy.

The ultrastructure of the thymus in the chick (Gallus domesticus) was studied after unilateral vagotomy at survival times of 3, 7 and 10 days. Ultrastructural changes in the ipsilateral thymus were observed in axon boutons as well as in myoid and cystic cells in the medulla, especially those situated near the corticomedullary junction. Structural changes in axon boutons ranged from granular degeneration of the axonal cytoskeleton to vacuolation of the axoplasm. Myelin figures of different sizes and configurations and clumping of small agranular vesicles were commonly observed in the axon terminals. Degeneration of myoid cells appeared to peak at 7 days post-vagotomy. Changes ranged from oedematous appearance and intense vacuolation of the peripheral cytoplasm to disorganisation and clumping of myofibrils. In some myoid cells the sarcomeres showed granular degeneration at the I-bands and in others, the myofibrils were completely degenerated such that amorphous material and partially degenerated organelles filled the entire cell. The majority of cystic cells at 3 days post-vagotomy showed a uniform increase in electron density. Numerous electron dense bodies, some displaying concentric lamellation, were observed throughout the expanse of the cytoplasm. At 7 days post-vagotomy, the cytoplasm of some cells gave a "moth-eaten" appearance. Dying cystic cells were encountered at 10 days after vagotomy. Degeneration in the myoid and cystic cells suggests that these cellular components may be the putative targets of the vagal fibres in the chick thymus. The changes in these cells reflect a disturbance in the cell metabolism presumably brought about by the removal of vagal influence.

Effects of BDNF and NT-3 on hair cell survival in guinea pig cochlea damaged by kanamycin treatment.

The aim of this study was to determine whether neurotrophic factors such as brain derived neurotrophic factor (BDNF) and neurotrophin 3 (NT-3) would protect auditory hair cells from ototoxicity by aminoglycoside antibiotic. Twenty-seven Wistar guinea pigs were divided into three groups of nine animals each. BDNF and NT-3 (100 microg/ml) were delivered into the right scala tympani of guinea pig cochlea through a cannula-osmotic pump device. Artificial perilymph (AP) was used as control. Immediately after implantation of the device, each animal was given five successive doses of kanamycin (400 mg/kg). At 15, 30 and 60 days after infusion, surviving inner and outer hair cells were counted at each turn of every cochlea with a Philips 515 scanning electron microscope. Multiple comparison tests were carried out among the groups, using ANOVA and Dunnett T3/Tukey HSD. Protective effects of NT-3 on hair cells were observed at 30 and 60 days after kanamycin injection. BDNF had no protective effect on hair cells at 15 and 60 days, but some at 30 days. This study suggests that NT-3 and BDNF may protect against cochlear hair cell damage caused by kanamycin treatment. Possible mechanisms for the otoprotective effects were discussed. No single mechanism postulated can explain fully the results seen in this study. It is possible that the mechanisms act in concert to produce the observed effects, or there are as yet undiscovered mechanisms or secondary messengers responsible for the otoprotective effects.

Time-course and localization of transferrin receptor expression in the substantia nigra of 6-hydroxydopamine-induced parkinsonian rats.

Parkinson's disease is a neurodegenerative disease characterized by dopaminergic cell death in the substantia nigra. The cause of the cell death is, however, obscure. Recently, accumulation of iron in the parkinsonian substantia nigra and iron-catalysed free radical generation have been proposed as possible causes of nigral cell death. The transferrin receptor has been implicated as a possible mediator of this iron accumulation in the parkinsonian substantia nigra. The present study investigated the distribution of transferrin receptor-immunoreactive proteins and its co-localization with tyrosine hydroxylase in the normal rat substantia nigra and their expressions in the parkinsonian substantia nigra from three days to three months after 6-hydroxydopamine lesioning. Computer image analysis of the grey mean of transferrin receptor staining in the microvessels was also employed. The results showed that the transferrin receptor immunolabelling was localized in some neurons and glial cells in the normal substantia nigra pars compacta and pars reticulata, and that about 54% of tyrosine hydroxylase-positive cells were also stained with transferrin receptor. There was a decrease of tyrosine hydroxylase- and transferrin receptor-positive cells in the 6-hydroxydopamine-lesioned substantia nigra. The grey mean of transferrin receptor staining in microvessels in the lesioned substantia nigra was, however, not different from that in the control. It was concluded that transferrin receptors in neurons, glial cells and microvessels might not be responsible for iron accumulation in the parkinsonian substantia nigra. The loss of transferrin receptor-immunopositive cells might, however, partly be accounted for by the death of transferrin receptor-positive dopaminergic cells induced by 6-hydroxydopamine lesioning.

Apolipoprotein D gene expression in the rat brain and light and electron microscopic immunocytochemistry of apolipoprotein D expression in the cerebellum of neonatal, immature and adult rats.

Apolipoprotein D gene and protein expression were investigated in the rat brain and cerebellum, respectively, during development. Apolipoprotein D gene expression was first observed in embryonic day 12 rat brain, with a moderate increase in apolipoprotein D messenger RNA levels towards the later part (embryonic days 15-17) of gestation. In the postnatal rat brain, a marked induction of apolipoprotein D messenger RNA occurred at postnatal day 10, with progressively higher levels of apolipoprotein D messenger RNA observed up to postnatal day 20. Somewhat lower, but none the less high, levels of apolipoprotein D messenger RNA continued to be present in brains of adult animals. In the immature cerebellum (day 3 up to one- to two-week-old rats), there were many densely labeled apolipoprotein D-immunoreactive cells that had features of oligodendrocyte precursors. Purkinje neurons showed apolipoprotein D immunoreactivity in one- to two-week-old animals, after which there appeared to be some decrease in staining. Oligodendrocytes in the cerebella of two-week-old animals were strongly apolipoprotein D positive, with immunoreactivity declining in older animals. These results reveal a maturation-associated induction of apolipoprotein D gene expression in the rat brain, and expression of apolipoprotein D in glial (immature oligodendrocyte) cells in the immature cerebellum, followed by specific expression of apolipoprotein D in Purkinje neurons.

Capturing the sublimity of a free radical gas.

This paper reviews the work related to nitric oxide (NO) done by the author and his postgraduates and colleagues in the past 7 years in the National University of Singapore. Our work shows that (i) NADPH-d and NO synthase (NOS) are often but not always identical; (ii) NO (as indicated by NADPH-d histochemistry and NOS immunohistochemistry) is generated in some endocrine (thyroid, parathyroid and ultimobranchial glands) and immune (thymus and bursa of Fabricius) organs and the cochlea. It is noted from the above studies that NO could possibly regulate blood flow through the various organs via its presence in the vascular endothelial cells and also via nitrergic neurons innervating the blood vessels. It could also regulate the activity of the secretary cells of these organs by being present in them, as well as acting through nitrergic neurons closely related to them. The paper also examines the Janus-faced nature of NO as a neuroprotective and neurodestructive agent, and the apparent noninvolvement of peroxynitrite and inducible NOS in neuronal death occurring in the red nucleus and nucleus dorsalis after spinal cord hemisection.

Induction of microglial reaction and expression of nitric oxide synthase I in the nucleus dorsalis and red nucleus following lower thoracic spinal cord hemisection.

In the present study, immunohistochemical stainings for OX-6, OX-42, nitric oxide synthase I and II as well as nitrotyrosine were used to investigate possible correlation among microglial reactivity, nitric oxide synthase upregulation, peroxynitrite involvement and neuronal death in the nucleus dorsalis and red nucleus following lower thoracic spinal cord hemisection. Significant neuronal loss was found in the ipsilateral nucleus dorsalis and contralateral red nucleus after cord hemisection. A distinctive microglial reaction for OX-42 could be observed from one to four weeks post axotomy in the ipsilateral nucleus dorsalis; by contrast, it was observed on both sides of the red nucleus from one to three weeks following cord hemisection. The activated microglial cells showed some degree of hypertrophy. From the microglial immunoreactivity as well as their appearance, it was speculated that microglial activation might be beneficial or protective to the axotomized neurons. In normal and sham-operated rats, neurons of the nucleus dorsalis were not nitric oxide synthase I reactive. Three weeks after cord hemisection, neurons in the ipsilateral nucleus dorsalis below the lesion showed strong immunoreactivity. Neurons in the red nucleus that normally displayed weak nitric oxide synthase I immunoreactivity showed an increase on both sides of the nucleus. These results suggested that nitric oxide synthase I expression in the nucleus dorsalis following axotomy was synthesized de novo and might act as a neurotoxic agent. However, the bilateral increase in expression of nitric oxide synthase I in the red nucleus after lower thoracic cord hemisection was due to up-regulation of the constitutive enzyme and might have some neuroprotective function. Our results also suggested that peroxynitrite played no or little role in the neurodegeneration in the nucleus dorsalis and red nucleus following axotomy.

Effects of interleukin-3 injection on supraventricular amoeboid microglial cells in neonatal BALB/c and athymic mice.

The present study investigated the effects of interleukin-3 (IL-3) on supraventricular amoeboid microglial cells (SAMC) of neonatal BALB/c and athymic mice. After four consecutive daily intraperitoneal injections of IL-3 at the age of 1 day postnatum and perfusion at the age of 5 days, BALB/c and athymic mice showed a 20% and 37% increase, respectively, in the number of Mac-1 positive SAMC. In mice receiving seven successive injections of IL-3 and perfused at the age of 8 days postnatum, Mac-1 labelled SAMC were increased by 14% and 19%, respectively. The increased number of SAMC could be the result of cytokine stimulation of their progenitor cells, viz., the stem cells of bone marrow or monocytes, or the result of direct stimulation of the SAMC themselves.

Effect of 6-OHDA injection on the AMPA glutamate receptor subunits in the substantia nigra of Sprague-Dawley rats.

Parkinson's disease (PD) is characterized by the destruction of dopaminergic cells in the substantia nigra (SN). The cause of the cell death and the development of Parkinsonism is however unknown. There are increasing evidences to suggest the involvement of glutamate mediated by its receptors. Using immunohistochemistry and cell counting, the present study investigated whether the numbers of neurons immunostained with glutamate alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptor subunits GluR1, GluR2/3 and GluR4 in the SN of rats would change after the injection of 6-hydroxydopamine (6-OHDA) into the SN. The results showed that the numbers of GluR1 positive cells were significantly decreased in the substantia nigra pars compacta (SNc), pars reticulata (SNr) and pars lateralis (SNl) from 3 days (13.7%) to 3 months (40.3%) and of GluR2/3 cells, from 1 week (17.6%) to 3 months (19.1%) after 6-OHDA injection, compared to those in the contralateral non-injected side. There was, however, no significant difference in the number of GluR4 positive cells between the injected and non-injected SN. The results were discussed.