The results showed high correlations between SOL and GL in pretest (r = 0.803, P < 0.01) and posttest (r = 0.770, P

< 0.01). The GL and GM were highly correlated in pretest (r = 0.818, P < 0.01) and posttest (r = 0.847, P < 0.01). Furthermore, there were medium correlations between GM and SOL in pretest (r = 0.671, P < 0.05) and no significant correlations in posttest (r = 0.595, P > 0.05). Comparing the regression lines of SOL pretest versus GL pretest with SOL posttest versus GL posttest, one can see a shift to the left upper side. This can be ascribed to the decrease in GL check details activity and the increase in SOL activity as indicated exemplarily by one participant (Fig. 3, gray arrow). Figure 3 Inhibitors,research,lifescience,medical Correlations of the electromyography (EMG) activity of m. gastrocnemius lateralis (GL) and m. soleus (SOL) in pretest (open circles) and posttest (filled circles), respectively. The regression lines are presented for EMG activity of GL and SOL in pretest … Discussion This is the first study that demonstrated an Inhibitors,research,lifescience,medical increase in synergistic EMG activity during maximal voluntary isometric

contractions following NMES Inhibitors,research,lifescience,medical of one muscle. Due to the NMES of the GL, the EMG activity decreased to 81% in posttest. This decline was compensated by the EMG activity of SOL that increased to 112% in posttest. The force during MVC did not change significantly after NMES of the GL (Fig. 2D). Following sustained NMES of the GL, voluntary GL muscle activity during maximal Inhibitors,research,lifescience,medical isometric contractions was reduced (Fig. 2A). The results are in line with other studies that found decreased EMG amplitudes after high-frequency NMES (Boerio et al. 2005). The decline in EMG activity occurs due to failure of electrical propagation at the muscle fiber membrane of the GL induced by high-frequency fatigue (Cairns and Dulhunty 1995; Badier et al. 1999). Furthermore, studies using the interpolation Inhibitors,research,lifescience,medical twitch technique showed that electrical stimulation of the triceps surae lead to central fatigue (Boerio et al. 2005) accompanied by a force decline. In our studies, the force did not change significantly

(P = 0.388) after NMES of the GL. For that reason, we assume that the decline in GL in the presented study occurred more prominently due to peripheral fatigue than due to central fatigue (Badier et al. 1999). Reducing knee angle leads to reduced GM length and decreased muscle activation during MVC (Cresswell et al. 1995; Arampatzis et al. 2006). This may be due to (1) nearly the “drive,” i.e., the neural outflow from spinal motor neurons, may be reduced to a shortened muscle; (2) neuromuscular transmission–propagation in a shortened muscle may be impaired, and (3) shortening a muscle may alter the electrode configuration with respect to the recording volume, thereby resulting in less myoelectric activity recorded (Cresswell et al. 1995). In our experiments, knee and ankle angle and therefore the muscle length were kept constant during pre- and posttests.

Similar to prostate cancer where expression OATP1B3 is significantly related to the Gleason score as a marker for tissue dedifferentiation [5], higher OATP1B3 levels in colon are associated with earlier tumor stage and they are found in better differentiated tumors. However, they are not predictive for the 5-year survival and for tumor recurrence. Within lower Inhibitors,research,lifescience,medical tumor grades, OATP1B3 expression is associated with an improved 5-year survival, while the tumor ABT-263 chemical structure recurrence in patients with poorly differentiated tumors is independent on

the expression of this OATP [16]. 7. OATP Expression in Pancreatic Cancer Extensive research has failed to produce any therapy efficient enough to substantially extend the median survival of treated patients beyond 6 months. Currently available therapies remain palliative on their intent [33–35]. Therefore, identification of new molecular targets and discovery of novel targeted therapies is of top priority for pancreatic cancer research. In a recent study, the expression of OATP1A2,

Inhibitors,research,lifescience,medical OATP1B1, and OATP1B3 was studied by immunohistochemistry in a sample of 12 patients as well as on the mRNA level in two pancreatic cancer cell lines [17]. Quantitative analysis was done by the Inhibitors,research,lifescience,medical HistoQUEST Software using the TissueFaxs Microscopic Image Analysis System (TissueGnostics, Inhibitors,research,lifescience,medical Vienna, Austria). The three studied polypeptides were found ubiquitously expressed in all studied pancreatic cancer biopsy samples. Methods used confirmed extensive immunostaining of the entire cancer cell tissue with the antibodies against these OATPs. In detail, the OATP1A2 expression signal was weak in one sample and moderate to strong in all others. OATP1B1 was found to be weakly expressed in all 12 cases. Immunostaining with the mMDQ antibody against OATP 1B1/1B3 was proved to be the most intense. Nine cases demonstrated moderate expression and three cases stained strong. OATP 1B1 and 1B3 mRNA expression Inhibitors,research,lifescience,medical in

two cell lines, MIA PaCa-2 and Bx-PC3, was comparable to that in normal liver, which was taken as a control, all because both of these transporters are considered “liver-specific”. Their mRNA expression, however, in normal pancreas was either undetectable (OATP 1B1) or 30–60 times lower than that in normal liver (OATP 1B3). The OATPs investigated in this study were all found to be ubiquitously expressed at the protein and the mRNA level which flags them as appropriate candidates for in vitro studying of OATP-targeted anticancer compounds [17]. 8. OATP Expression in Liver Cancer In tumors of the liver, the expression of OATP1B1 and OATP1B3 is reduced along the degree of tissue dedifferentiation. This could reflect the reduction of metabolic function of liver cells in more advanced tumors [5].

, UK. All in vivo procedures were carried out in compliance with the United Kingdom Animal (Scientific Procedures) Act 1986 and associated Codes of Practice for the Housing and Care of Animals. Preparation of the HEC based RSV formulations has been described previously [13]. Briefly, a HiVac® Bowl (Summit Medical Ltd., Gloucestershire, UK) was used to facilitate mixing under vacuum following the stepwise

addition of components. Poylcarbophil (PC) (3% w/w) was first added to the bowl containing deionised water and sodium hydroxide prior to the addition of HEC (3 or 5% w/w) followed by polyvinylpyrollidone (PVP) (4% w/w). PC (3% w/w) was added to the vortex produced in a metal beaker by rapid stirring (at 500 rev min−1) of deionised water and the required amount of NaOH to reach pH 6 using a Heidolph mechanical stirrer. Following complete dissolution of the mucoadhesive component, NaCMC (3, 5 or 10% w/w) and PVP (4% w/w) were added stepwise following attainment of homogeneity. 5FU The gels were transferred to sterile centrifuge tubes, gently centrifuged and stored for 24 h (ambient temperature) prior to analysis. Flow rheometry was conducted using an AR2000 rheometer (T.A. Instruments, Surrey, England) at 25 ± 0.1 °C using a 6 cm diameter MI-773 parallel plate geometry (selected according to formulation consistency) and a gap of 1000 μm, as previously reported [12]. Flow curves

(plots of viscosity versus shear rate) were examined in the range of 0.1–100 s−1. NaCMC semi-solid (2.8 g) was weighed into a 5 ml syringe barrel. The semi-solid loaded syringe barrel was attached to a second syringe via a 1.5 cm length of Nalgene tubing. CN54gp140 (200 μl at 530 μg/ml) was added to the semi-solid containing syringe barrel via pipette and the plunger replaced. Uniform distribution of CN54gp140 throughout the semi-solid formulation was achieved by carrying out 40 passes of the syringe barrel contents from one syringe to the other (method previously validated [13]). Semi-solids (HEC- and NaCMC-based) (0.36 g) were weighed into a speed mixing pot prior

to the addition of CN54gp140 (180 μl at 3.5 mg/ml). 2 Spin cycles at 3300 rpm for 30 s were carried out to provide uniform antigen distribution throughout the semi-solid not formulations. The same lyophilization protocol was adopted for each formulation. To optimise the lyophilization protocols, the glass transition temperatures of the selected and cooled semi-solid formulations were investigated by DSC using hermetic pans (DSC Q100, TA Instruments, Surrey, UK). Following cooling to −60 °C and holding isothermally for 5 min, the samples were heated at 2–40 °C using a modulated procedure (±0.4 °C every 0.5 s). Prior to lyophilization, semi-solid formulations were dispensed into suitable blister packs using a TS250 Digital Timed Dispenser (Adhesive Dispensing Ltd., Buckinghamshire, UK) for tablet Modulators formation or alternatively extruded into nalgene tubing with the use of a 5 ml syringe for rod formation.

In Norway, a train accident near Aasta killed 19 people whereas 67 passengers survived. Approximately 600 personnel from different 11 services participated in the initial management of this major incident [25]. A review of the World Trade Center attack in 2001 concluded that “the lack of communication resulted in more problems than all other factors combined” [26]. Further, during a major aircraft incident in UK, the simultaneous use of

several different triage-labelling systems contributed to confusion [27]. A triage concept with uniform instructions and standardized triage tagging would alleviate on-scene confusion and national standards has been called Inhibitors,research,lifescience,medical for both in the US and Australia [14,28]. In Norway, the lack of a standard major incident triage concept that is nationally accepted, reliable and validated remains a gap in our major incident preparedness. Conclusions Major incident triage skills can be effectively taught to multi-disciplinary emergency service professionals using a combination of lectures and practical simulations in a two-day course. Our Inhibitors,research,lifescience,medical modified triage Sieve tool provides acceptable accuracy in allocating priority during simulated

major incidents and may serve as a candidate for a future national standard for major incident triage. Competing interests Declared. The TAS-courses are funded and organized by the Norwegian Inhibitors,research,lifescience,medical Air Ambulance Foundation. Trond Vigerust is a hired consultant for Inhibitors,research,lifescience,medical LESS, a manufacturer of emergency stretchers. All other authors declare no conflict of interest. Authors’ contributions MR, HML, AJK, TV and JEA conceived the study. MR, AJK, TV and JEA designed the study. JEA supervised the data collection. TV, AJK and MR managed the collected data. MR performed the analysis and drafted the manuscript. All authors interpreted data and critically revised the manuscript. All authors have read and approved the final manuscript. Pre-publication history The pre-publication history for this paper can be accessed here: http://www.biomedcentral.com/1471-227X/10/17/prepub Inhibitors,research,lifescience,medical Supplementary Material Additional file 1: Example of patient information card. Status

inside bus wreck and at casualty clearing station. Click here for file(427K, PPT) Additional file 2: Questionnaire. Word file containing questionnaire (in Norwegian language). Click here for file(307K, DOC) Acknowledgements We acknowledge mafosfamide and thank Torfinn Hallerud, Bent Krister Osbakk, Kai Tangen, Børre Østby and Janne Lisbeth Støylen Bådholm for their willingness to participate and support this http://www.selleckchem.com/products/Pomalidomide(CC-4047).html project, and for their continued dedication to improved inter-disciplinary management of major incidents. We thank Prehospital Katastrofmedicinsk Centrum, Gothenburg, Sweden for friendly advice and thoughtful input. We thank Lars Erik Vollebæk for assistance with graphical design. We are grateful to all emergency service professionals participating in a TAS-course.

Using 1.5T MRI the gyral pattern (agyria or pachygyria), thickened cortex and other brain abnormalities can readily be appreciated.75 Several different patterns of LIS arc recognized using MRI, which led to development of a detailed grading system78,79 which considers both the severity of the gyral pattern simplification and the gradient along the anterior to posterior axis. Most patients have a posterior to anterior (P>A) gradient in which the gyral malformation is more severe posteriorly than anteriorly. This pattern is seen most, often as a consequence of a mutation in the LIS1 gene, but

may also occur with mutations of TUBA1A. 80 Others have the reverse anterior to posterior (A>P) gradient, Inhibitors,research,lifescience,medical Inhibitors,research,lifescience,medical which is seen most commonly as a consequence of mutations in the DCX gene. selleck chemicals llc Figure 4 shows the imaging features of the two main gradients of LIS, and Figure 5 shows different grades of LIS severity. Figure 4. Imaging features of classical lissencephaly contrasting the P>A gradient with the A>P gradient. Axial T1 -weighted MRI scans. The image on the left shows near-complete agyria posteriorly transitioning to pachygyria anteriorly. This is … Figure 5. Imaging features of classical lissencephaly showing the four severity grades. All images are T1 – or T2 -weighted MRI scans. The top row shows axial scans and the

Inhibitors,research,lifescience,medical bottom row coronal scans. Grade 1 is near complete agyria, grade 2 is posterior agyria and … Six genes associated with LIS syndromes have been identified, and in approximately Inhibitors,research,lifescience,medical 80% of cases, a genetic cause can be found, usually an abnormality of the LIS1 or DCX genes.78,81 The six known genes associated with causation of LIS

are LIS1,82 DCX,83 ARX,70 RELN,69 YWHAE,76 and TUBA1A 84 These genes are all known to be required for optimal migration of neurons during brain development. All but the ARX gene are required for normal radial migration of neurons whereas the ARX gene is required for normal tangential migration.85 Inhibitors,research,lifescience,medical Mutations in the LIS1 gene are the most common cause of LIS.81 The LIS1 protein is not only required for neuronal migration, but. it is also required for cellular proliferation and intracellular transport (reviewed in ref 86). Subcortical band heterotopia Subcortical band heterotopia (SBH) is alternately known as double cortex87 or subcortical laminar heterotopia.88 The term SBH is preferable to double cortex, as the heterotopic gray matter lacks Thalidomide cortical lamination and organization, and does not resemble a cerebral cortex other than being composed of gray matter. SBH is characterized microscopically by bilateral bands of heterotopic gray matter located in the white matter between the lateral ventricular walls and the cortex.65 The overlying cortex appears normal with the exception of mildly shallow sulci. In the most typical forms, the bands are bilateral and symmetric and slightly more prominent anteriorly.

75-77 These findings are consistent with the hypothesis that induction of BDNF contributes to the neurogenic and behavioral find more actions of antidepressants. Other neurotrophic/growth factors There

is now strong evidence demonstrating a role for several other growth factors in the actions of stress, depression, and ADT, including vascular endothelial growth factor (VEGF), fibroblast growth factor 2 (FGF2), and insulin-like growth factor 1 (IGF-1). VEGF was originally characterized Inhibitors,research,lifescience,medical as a vascular permeability factor and an endothelial cell mitogen,101 but is also expressed in the brain in both neurons and glia, and has been shown to play a role in hippocampal neuroplasticity, memory, and neurogenesis.102,103 Inhibitors,research,lifescience,medical Chronic unpredictable stress decreases the expression of VEGF, as well as its receptor, Flk-1,102 while ADT increases VEGF expression in the granule cell layer

of the hippocampus.104 Different classes of chemical antidepressants, including SSRI, NSRI, and ECS, increase VEGF expression in the hippocampus, indicating that VEGF is a common downstream target of these treatments. The opposing Inhibitors,research,lifescience,medical actions of stress and ADT on VEGF suggest a possible relationship between neurogenesis and behavior. Stress has a greater effect on newborn cells associated with endothelial cells than nonvascular associated cells.102 In addition, VEGF is sufficient to induce neurogenesis and produce antidepressant effects in behavioral models of depression, whereas inhibition of Flk-1 blocks the induction of adult neurogenesis and the behavioral effects of ADT.104 A recent postmortem study Inhibitors,research,lifescience,medical found that the expression of FGF2 and its receptors (FGFR2 and FGFR3) are reduced in the PFC and cingulate cortex of MDD patients,105 and social

defeat stress decreases FGF2 Inhibitors,research,lifescience,medical in the hippocampus.106 Conversely, chronic ADT increases the expression of FGF2 in cerebral cortex and hippocampus of rodents107,108 and FGF2 infusions are sufficient to produce an antidepressant response in behavioral models.109 The role of FGF2 in the proliferative actions of ADT, on both neurons and glia, is currently being investigated. The expression of IGF-1 in the hippocampus is increased by chronic Carnitine palmitoyltransferase II administration of two different monoamine oxidase inhibitor antidepessants.110 In addition to expression in brain, circulating IGF-1, derived primarily from the liver, is actively transported into the brain and is required for the induction of neurogenesis in response to exercise,111 Recent studies have also demonstrated that IGF-1 administration, or agents that increase IGF-1 levels, produce antidepressant-like actions in behavioral models of depression.98,112,113 Together, these findings suggest that peripheral production and/or the central actions of IGF-1 could be novel targets for the treatment of depression.

In 1993,44 the group reported results from 96 patients who were admitted to an open trial of clozapine for treatment-resistant schizophrenia at the University

Hospital of Cleveland, and demonstrated that quality of life scores only improved in patients who continued clozapine treatment for at least 2 years, which means an improvement of 242%. Rosenheck et al16 conducted a comparative study of clozapine and selleckchem haloperidol in refractory schizophrenic inpatients. They carried out a randomized, 1-year double-blind study at 15 Veterans Affairs medical centers. A total of 423 patients (clozapine = 205 and haloperidol = 218) Inhibitors,research,lifescience,medical were assessed using the QLS.35 After 1 year, 117 clozapine-treated patients and 61 haloperidol-treated patients continued their assigned treatment. In these patients, clozapine was significantly better than haloperidol in improving patients’ quality of life. In 1996, Essock et al17 failed to find superiority of clozapine over conventional Inhibitors,research,lifescience,medical antipsychotics on patients’ quality of life. Their study was the Inhibitors,research,lifescience,medical first randomized costeffectiveness trial of clozapine. It was a 2-year open-label randomized study comparing clozapine with usual care in schizophrenic

or schizoaffective treatment-resistant inpatients. A total of 227 patients (138 in the clozapine group and 89 in the usual care group) were assessed using the Quality of Life Interview (QoLI).14 Clozapine did not significantly affect patients’ quality of life. By the 8th month of treatment, both groups experienced equivalent improvements in the QoLI global satisfaction score. Olanzapine Hamilton et al23 evaluated the impact of treatment with olanzapine compared with haloperidol and placebo on quality of life in schizophrenic inpatients. Inhibitors,research,lifescience,medical They conducted a double-blind randomized study, with a 6-week acute phase and an extension Inhibitors,research,lifescience,medical phase of 46 weeks for the responders. A total of 335 patients were randomized to one of the following groups: olanzapine 5±2.5 mg/d, olanzapine 10±2.5 mg/d, olanzapine 15±2.5 mg/d, haloperidol 15±5 mg/d, and placebo. Data at extension

week 24 was reported in their paper. Quality of life was assessed employing the QLS.35 At end point, no significant changes in the QLS total and subscale scores were observed for the placebo, olanzapine low-dose, or haloperidol groups. Moreover, significant improvements were Phosphatidylinositol diacylglycerol-lyase observed for olanzapine medium and high doses. The olanzapine medium-dose group demonstrated significant greater improvements in all QLS scores than the placebo group. The olanzapine high-dose group showed greater improvement in QLS total score compared with the placebo treatment group. The impact of olanzapine on quality of life has also been compared with the impact of haloperidol in a 6-week, double-blind randomized multicenter trial with a longterm extension (46 weeks).

These NAA measures reflect neuronal integrity and metabolism whereas changes in glutamate-glutamine-GABA metabolites may reflect changes in membrane structure, glial functions, and glutamate content. Together, the above data suggest that structural and metabolic alterations observed in vivo may be related to alterations in cell viability, which, itself, may be related to alterations in cell number, density, and size observed in postmortem tissues at the microscopic level.

The studies reviewed above undeniably prove the usefulness of postmortem tissue in unraveling the microscopic anatomical substrate of depression. For the first Inhibitors,research,lifescience,medical time, postmortem cell-counting studies in mood disorders have established that MDD and BPD are brain diseases with unique pathological alterations in neuronal and glial cells. The precise region- Inhibitors,research,lifescience,medical and layer-specific alterations in neuronal and glial architecture observed in mood disorders are consistent with the hypotheses of specific dysfunction in monoamine, glutamate, and GABA neurotransmitter systems in these disorders. Moreover, colocalization of cellular changes detected in postmortem tissues with in vivo neuroimaging findings proves that postmortem studies provide an important interface Inhibitors,research,lifescience,medical between clinical and basic research in unraveling the ncuroanatomical substrates of depression. Postmortem

studies in depression also indicate that while MDD and BPD are clearly not neurodegenerative disorders, these disorders are associated with impaired cellular neuroplasticity and resilience. It remains to be fully elucidated Inhibitors,research,lifescience,medical to what, extent these findings represent neurodevelopmental abnormalities, progression of the disorder, biochemical changes (in glucocorticoid or trophic factors levels) accompanying repeated disease episodes, or the results of treatment with therapeutic medications. Inhibitors,research,lifescience,medical It is unknown whether the cellular changes observed postmortem in mood disorders can be reversed by antidepressant and mood-stabilizing medications. this website Although molecular and genetic mechanisms associated with depression Linifanib (ABT-869) are yet to be unraveled, preliminary microarray studies of

gene expression in postmortem brain tissues from subjects with mood disorders confirm that the dorsolateral prefrontal and anterior cingulate cortex are sites of pathology in mood disorders.93,94 Selected abbreviations and acronyms AVP arginine-vasopressin BDNF brain-derived neurotrophic factor BPD bipolar disorder CRH corticotropin-releasing hormone GABA γ-aminobutyric acid GFAP glial fibrillary acidic protein HPA hypothalamic-pituitary-adrenal (axis) MDD major depressive disorder NAA N-acetylaspartate NMDA N-methyl-D-aspartate Notes The authors acknowledge the support of the National Alliance for Research on Schizophrenia and Depression, and Public Health Service Grants MH60451, MH61578, MH63187, MH67996, and P20 RR17701.

This systematic review found that recent studies focusing on exercise program adherence in older adults have used a variety of methods to measure adherence. There is no agreed method of assessing adherence to exercise among older people, so various approaches are used, making the comparison of adherence rates between studies difficult. This hampers progress toward understanding exercise adherence in older people, as well as how to enhance it. Adherence to centre-based exercise programs is relatively easy to document but adherence to home-based exercise currently relies on self-report, which may overestimate or underestimate actual exercise frequency and duration. In the future,

technology may enable more accurate Luminespib in vitro measurement of adherence in home-based physical activity studies. Given the variability in measurement of adherence it was not possible to meaningfully compare adherence rates across studies. inhibitors However, it was noted that retention and adherence rates in most of the included studies were suboptimal. The apparently higher rate of adherence to centre-based programs provides challenges for the widespread

implementation of exercise programs. Some programs combine group and home-based aspects. This may be a feasible and cost-effective solution. Given the limitations of this review, this issue requires further investigation. A number of person-level factors were found to be associated with greater adherence rates. Interestingly, reduced mental wellbeing appeared to present a greater barrier to exercise adherence than reduced physical wellbeing.10 People at risk of depression were less likely crotamiton AC220 to adhere to prescribed programs. Physical activity is potentially beneficial

for fatigue and depression, so future intervention could specifically target adherence in this group of people. The concept of loneliness also requires more investigation. This group of people might require more encouragement, affirmation and feedback.11 and 12 Adherence is promoted by the belief that an intervention will be effective (the outcome expectancy), as well as the belief that the individual is capable of following the requirements of the intervention (the efficacy expectancy).13 It has been postulated that people with greater adherence may engage in other health-promoting behaviours. Thus, adherence may be a marker for a personality type, or related to motivation or goal-directed behaviours. Self-efficacy, which may relate to motivation, is the perceived confidence in one’s ability to accomplish a specific task.13 Self-efficacy has been shown to affect exercise adoption and maintenance.11 Therefore, intervention programs should develop and nurture this characteristic to enable individuals to continue with the program. Several of the studies included in this review used a range of strategies in an effort to enhance adherence.

The evidence

for protective immunity, natural history and immunobiology of genital Ct infection in humans have also been extensively reviewed [10] and [11]. The authors concluded that more prospective studies in women with genital chlamydial infection are needed to inform development of a safe and effective chlamydial vaccine, but pointed out that these are logistically and ethically very difficult to do [5] and [11]. C. trachomatis also infects the human eye, causing trachoma, the leading infectious cause of blindness [12], [13] and [14]. The genomes of Ct strains isolated from the eye and genital tract are more than 99% identical [15], and the clinical and pathological findings of ocular and genital infection are similar. Infections are often asymptomatic at both sites, and are characterised by inflammation and the presence of sub-epithelial lymphoid follicles. The damage in both learn more the eye and genital tract Libraries results from fibrosis, which progresses slowly (over months or years) at the site of inflammation. The eye is more accessible to examination and sampling

than the urethra, cervix or fallopian tubes. There is an extensive literature on the natural history, immunology and pathogenesis of human ocular Ct infection. Human challenge studies, detailed selleck chemicals studies on the natural history, pathogenesis and immune response to experimental ocular infection in humans and non-human primates, and the results of several major trachoma vaccine trials in humans were reported in the 1960s. More recently there have been many publications on the immunological correlates of protective immunity and immunopathology following ocular Ct infection in humans, on the genetics of susceptibility to the scarring sequelae of ocular infection, and on gene expression at the site of infection those in the conjunctival epithelium [16]. The purpose of this review is to summarise the state of knowledge concerning the natural history, immunology and pathogenesis of ocular Ct infection in humans and non-human

primates (NHPs), for the benefit of those interested in the development of a vaccine against Ct; and to suggest how a chlamydial vaccine might be evaluated in humans. Human volunteer studies showed that the follicular keratoconjunctivitis characteristic of trachoma develops within 2–15 days of inoculation, depending on the dose inoculated, and resolves over several months [17] and [18]. The follicles of trachoma are best seen in the conjunctiva of the everted upper eyelid (the subtarsal conjunctiva) and, according to the World Health Organisation case definition, follicular trachoma (TF) is present when more than 5 follicles of >0.5 mm diameter are seen in the central area of the subtarsal conjunctiva.