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Biomedical subjects

H E Webb

Publications and source records attributed to H E Webb.

At least 19 recordsLinked to original sources
PubMed2006

Cardiorespiratory responses of Hi Fit and Low Fit subjects to mental challenge during exercise.

The influence of psychological states on physiological responses during exercise is of considerable importance to individuals for which the efficiency of energy production is critical to occupational performance. Numerous studies have shown that aerobic fitness is associated with enhanced cardiovascular efficiency at rest and that responses to mental stress demonstrate evidence of increased sensitivity (relative increase in HR response) and enhanced efficiency (a decrease in absolute HR). However, the effect of aerobic fitness and its impact on cardiorespiratory (CR) responses to psychological stress during exercise has not been investigated. Therefore, the purpose of this study was three-fold; (1) to examine during exercise, anxiety, effort sense, and CR responses to a mental challenge, (2) to examine anxiety and heart rate (HR) responses from rest to exercise with mental challenge between below average fitness (Low Fit) and well-above average fitness (Hi Fit) individuals (exercising at similar relative intensities), and (3) to examine anxiety, effort sense, and CR responses of Low Fit and Hi Fit individuals to a mental challenge during exercise at a similar relative intensity. Twelve Low Fit and eleven Hi Fit subjects participated in two, 32-minute cycle ergometer rides at 65 % of VO2max. In the mental challenge condition (MCC), subjects rode while participating in mentally challenging tasks (Stroop Color-Word task and mental arithmetic) from min 6 to min 14 of the protocol. In the no mental challenge condition (NMCC), subjects exercised at the same intensity and duration without a stressor. Subjects were counter-balanced between fitness levels and condition. HR, VE, VE/VO2, RR, VO2, RER, effort sense (RPE), and state anxiety (SAI) were assessed at 5, 14, 24, and 30 min. SAI was also assessed at - 5 min before exercise and after 15 min of recovery. In addition, the NASA task load index (NTLX) was used to assess perceived overall workload. SAI increased significantly at 14 min in the MCC. NTLX scores indicated that the MCC was perceived as a greater overall workload. Furthermore, HR, VE, VE/VO2, and RR were significantly elevated during the mental challenge condition at 14 min. The Hi Fit subjects tended to respond to the dual stress of exercise and mental challenge with a relative increase in HR, while absolute HR was similar in both groups. An examination of fitness group differences revealed that SAI and NTLX were similar for Low Fit and Hi Fit subjects when exercising in the MCC, although, Hi Fit subjects demonstrated lower HR responses from 6 min to 14 min. VE, VE/VO2, and RR were similar for Low Fit and Hi Fit subjects. These results suggest that psychological stress during physical activity can exacerbate cardiorespiratory responses and suggests that factors that impact CR adjustment to mental challenge from resting baseline may differ from the factors that impact CR adjustment to mental challenge during exercise. Finally, fitness level attenuates HR and may attenuate additional cardiorespiratory responses while participating in a dual stress condition, of exercise and mental challenge.

Adult↗
PubMed1993

Effect of amitriptyline on neurotransmitter levels in adult mice following infection with the avirulent strain of Semliki Forest virus.

Infection of adult mice with the avirulent strain of Semliki Forest virus (SFV) led to neurochemical abnormalities, notably depressed levels of catecholamines (CATs) such as noradrenaline (NA), adrenaline (A) and 3-methoxy-4-hydroxyphenylglycol (MHPG) (a metabolite of NA) particularly in the hypothalamus and the inferior colliculus but not in the temporal cortex. In addition, depressed levels of NA and A were also found in the cerebrospinal fluid (CSF) and the serum. Administration of a tricyclic antidepressant drug, amitriptyline, kept the levels of NA, A and MHPG similar to those of the saline-treated control mice in the hypothalamus, inferior colliculus and CSF.

Amitriptyline↗
PubMed1992

IgG subclass responses in brain and serum in Semliki Forest virus demyelinating encephalitis.

The response of IgG subclasses within the central nervous system (CNS) of the mouse to Semliki Forest virus (SFV), an alphavirus associated with meningoencephalitis and primary immune mediated demyelination, has been measured using immunocytochemistry. The subclass response in serum has been assessed using virus specific enzyme linked immunosorbent assays. In the CNS IgG1 was poorly represented throughout the sampling period of 28 days with a maximum of 3% of the total number of positive cells on day 21 after infection. Of the few IgG positive cells present on day 6, 2a and 3 positive cells were dominant. From day 9 onwards the numbers of 2b positive cells rose and by day 28 IgG2a, 2b and 3 subclasses showed roughly equal percentages of total cells counted. By contrast, in serum, anti-SFV IgG 2a and 2b were the first to appear and were dominant on day 12 and 21. Levels of anti-SFV IgG1 did not rise until after day 12 but rose steeply thereafter. IgG3 was weakly positive at days 9 and 12, rising slightly on day 21. Clearly there are differences in the patterns of subclass response between the CNS and the periphery. This may be important in the context of neurotropic viral infection.

Animals↗
PubMed1990

Induction of membrane proliferation in mouse CNS by gold sodium thiomalate with reference to increased virulence of the avirulent Semliki Forest virus.

Separation of smooth membrane vesicles from whole mouse brain by isopycnic centrifugation in discontinuous sucrose density gradients show an increased membrane proliferation in gold sodium thiomalate (GSTM) treated mice. Induction of membrane proliferation by GSTM seems to be an important factor in converting the avirulent Semliki Forest virus infection into a lethal one.

Animals↗
PubMed1990

Immunoelectron microscopical labelling of a glycolipid in the envelopes of brain cell-derived budding viruses, Semliki Forest, influenza and measles, using a monoclonal antibody directed chiefly against galactocerebroside resulting from Semliki Forest virus infection.

Neurotropic RNA budding viruses such as Semliki Forest virus (SFV), influenza and measles were each grown in identical mouse brain cell cultures. Positive immunoelectron microscopical labelling with gold was seen in the envelope of these viruses using an anti-SFV derived glycolipid monoclonal antibody (MAb), 373 shown to be directed chiefly against galactocerebroside. The results indicate that each enveloped virus grown from the same cell type contains the same glycolipid in its envelope. The presence of common glycolipids derived from the host cell in the envelopes of various enveloped budding viruses may play a significant role in the pathogenesis of virus induced, immune mediated CNS autoimmunity and demyelination, particularly in multiple sclerosis (MS).

Animals↗
PubMed1990

The effect of gold sodium thiomalate and its constituent part, thiomalate, on the virus titres and the lysosomal enzyme activity in peritoneal macrophages of Swiss/A2G mice infected with the avirulent strain of Semliki Forest virus.

Treatment of adult mice with gold sodium thiomalate made the normally non-lethal Semliki Forest virus infection lethal. Associated with this was a significant increase in brain virus titre and a depression of peritoneal macrophage lysosomal enzyme activity. In contrast, treatment of adult mice with the constituent part, thiomalate, did not make the non-lethal Semliki Forest virus infection lethal. Brain virus titre and peritoneal macrophage lysosomal enzyme activity were comparable to the controls. The mechanism by which gold sodium thiomalate increases the virulence of Semliki Forest virus is discussed.

Acid Phosphatase↗
PubMed1989

Identification of immunoglobulin-containing cells in the central nervous system of the mouse following infection with the demyelinating strain of Semliki Forest virus.

Cells within the central nervous system were identified as containing immunoglobulin G, A and M using immunocytochemistry in mice previously infected with Semliki Forest virus, a togavirus causing primary immune-mediated demyelination. Cells positive for these immunoglobulins were counted in cerebellar white matter, parenchyma, meninges and choroid plexus/ventricles. No positively staining cells were seen on day 6 after infection although other inflammatory cells were present at this time and virus-specific immunoglobulin was found in serum. Cells positive for IgG appeared in all areas by day 9 and remained dominant in numbers throughout. IgM-secreting cells appeared in small numbers in the parenchyma first on day 9 and subsequently in other areas, their numbers rising to a maximum on day 12 in all areas and falling thereafter. The number of IgA-secreting cells was small. They appeared by PID 12 and continued to rise on successive sampling days. Initially IgG-positive cells were seen in the perivascular cuffs but by day 12 a few had moved away from the cuffs into the adjacent parenchyma. IgG-positive cells were seen both in and away from cuffs within areas of demyelination. IgM and IgA-positive cells tended to follow the distribution of IgG-positive cells, but in fewer numbers.

Animals↗
PubMed1988

Immunocytochemical evidence for Semliki Forest virus antigen persistence in mouse brain.

Semliki Forest virus (SFV) is neurotropic in mice. Mature virulent virus (strain L10) can be identified within the CNS by electron microscopy in adult mice. Inspite of high virus titres, avirulent SFV A7(74) cannot be visualised in the brain of adult mice. Immunocytochemical studies using monoclonal antibodies (MAbs) to A7(74) E1 and E2 proteins and viral envelope glycolipids, showed viral E1 to be labelled in the cerebral capillaries, the E2 and the putative envelope glycolipids were labelled in the cytoplasm of neurons, particularly in the hippocampal areas and glia in the cerebellum. By double labelling the presence of viral antigens in astrocytes and oligodendrocytes was demonstrated. Viral antigens were identified in the brain up to 183 days after infection. Paraffin sections from Bouin-fixed tissue were found to be the most suitable material for immunocytochemistry of SFV. The presence of life-long anti SFV antibody in the sera of animals after SFV infection, could be due to the persistence of viral antigens acting as constant stimuli to the immune system.

Animals↗
PubMed1988

An electron microscopical study of the replication of avirulent Semliki Forest virus in the retina of mice.

Electron microscopical (EM) studies were carried out on the retinas of 2-3-(baby), 12-, 14- and 21-28-day-old (adult) mice infected with avirulent (A774) Semliki Forest virus (SFV). Virions (mature virus), spherules and advanced stages of virus replication, cytopathic vacuoles type II (CPV II), were seen in the retinal neurons of baby mice after intracerebral (i.c.) or intraperitoneal (i.p.) infection. Some virions and spherules were also seen in the retinas of 12- and 14-day-old mice. Virions and advanced stages of virus replication were not seen in adult mice despite high virus titres. Some neurons of the inner nuclear layer and some ganglion cells showed reduced basophilia and appeared pale and occasionally some dense clumps of fine granules (DC) were seen in the neurones of the inner nuclear layer in these mice. A few small spherules were seen in the extracellular spaces. Some infiltrating cells were seen in the retinas in all ages of mice. We suggest that SFV causes retinopathy in baby mice and the neurophysiological changes reported in adult mice may be contributed to by virus replication in the retinal neurones and the presence of infiltrating cells in the retina.

Animals↗
PubMed1988

CNS pathogenesis following a dual viral infection with Semliki Forest (alphavirus) and Langat (flavivirus).

Mice inoculated intraperitoneally with the alphavirus Semliki Forest were protected against a subsequent challenge with the flavivirus Langat. The protection was seen as a reduction in the Langat virus titres, mortality index and percentage deaths. The severity of the brain pathology was greater in the simultaneously infected mice, or when the time interval between administration of the viruses was 7 days, compared to that seen following a single infection of either Semliki Forest or Langat virus. When the time interval was greater than 14 days the severity of the histopathological lesions were reduced. Two factors were considered to be of possible importance in the protection afforded by the original alphavirus. Either persistence of the alphavirus interfering with the challenge flavivirus or cross-reactive immunity arising from a common host cell membrane derived glycolipid component present in both viral envelopes. This latter phenomenon could be important as anti-glycolipid activity present at 14 days after the first virus increased significantly after challenge with the second virus.

Animals↗
PubMed1987

Cyclosporine enhances virally induced T-cell-mediated demyelination. The effect of cyclosporine on a demyelinating virus infection.

Semliki Forest virus infection of adult mice results in a demyelinating meningoencephalomyelitis. Demyelination does not result from direct viral damage but from the activity of T lymphocytes. We have studied the effect of the immunosuppressant cyclosporine (Cs) on the outcome of this infection. Cs had no effect when given 5 days after the infection, and little effect when given 4 h after infection. When the Cs was given 48 h before infection there was a prolongation of the blood and brain virus titres, and a reduction in some mice of serum IgG anti-viral antibody synthesis, but an increase in the severity of the CNS inflammatory response and the demyelination. Consideration of these findings along with measurement of Cs levels in the serum and cerebrospinal fluid suggests that this drug does not cross the blood brain barrier.

Animals↗
PubMed1987

Semliki Forest virus-induced, immune-mediated demyelination: adoptive transfer studies and viral persistence in nude mice.

Adoptive transfer experiments in athymic nude mice demonstrated that the demyelination seen in the central nervous system (CNS) following Semliki Forest virus (SFV) infection was directly dependent upon sensitized T lymphocytes. Antibodies generated during the infection did not seem to be involved in the demyelination, but thymus-dependent antibodies (IgG) were responsible for the reduction of brain virus titres. In the absence of a T cell response and T cell-dependent antibody production, virus persisted in the CNS for several months. Despite persistence of high virus titres for this time, only mice eventually developing a CNS inflammatory response developed lesions of demyelination. In the absence of an inflammatory response no demyelination was apparent even after several months of persistent infection. Administration of anti-SFV hyperimmune serum intracerebrally to both infected and control mice did not produce demyelination but resulted in CNS tissue degeneration with marked pycnosis.

Animals↗