1 Swift identification and management of mild hypoglycaemic episo

1 Swift identification and management of mild hypoglycaemic episodes prevent progression to severe hypoglycaemia2 which has been associated with increased morbidity,3,4 as has increased duration of hypoglycaemia.5,6 The majority of inpatients with Dasatinib nmr diabetes on nasogastric feeding have altered conscious state and are unable to respond to symptoms of hypoglycaemia, making them reliant on often busy staff, to identify and treat their hypoglycaemia. In this context, even with regular blood glucose monitoring (BGM) there may be considerable progression of a hypoglycaemic episode prior to its identification.5,6 There is extensive literature on diabetes specific formula feeds, mainly with regard to

post-feed hyperglycaemia,7 but less quantifying hypoglycaemia.8–10 We carried out a retrospective case note review to determine

the frequency and timing of hypoglycaemia in hospitalised patients with diabetes on established nasogastric feeding in a tertiary hospital. Subjects were 50 inpatients with diabetes (27 male, 23 female) fed entirely by nasogastric feeding for ≥3 days as per hospital protocol (Table 1). Patients on insulin infusions or in ICU were excluded. Subjects were consecutively flagged by the treating dietitian. Data were collected from medical notes, BGM records, and medication charts. Goals of treatment were blood glucose level (BGL) ≥4 and <10mmol/L. Initial treatment of hypoglycaemia was liquid carbohydrate as per hospital protocol. No identifying information was collected. The study was approved by the Human Ethics Research TSA HDAC ic50 Committee (Curtin University, Western Australia) and as a tertiary hospital clinical audit. Hypoglycaemia was defined as BGL <3.5mmol/L, as a level having clinical relevance.11,12 Severe hypoglycaemia is formally defined as ‘an event requiring assistance of another person to actively administer carbohydrate’;13 but as this was applicable to all events in this study, we arbitrarily defined severe hypoglycaemia as BGL <2.0mmol/L,

and extended hypoglycaemia as duration >2 hours or repeat episode within 2 hours. There Methane monooxygenase is no standardised reporting method for frequency of hypoglycaemia14 so we have reported it both as percentage of patient-days with ≥1 hypoglycaemic episode (PPD) and percentage of total blood glucose values <3.5mmol/L (PTG), to allow for variable feed duration and consistent with two other studies.8,9 Descriptive statistics were used for subject demographics, χ2 test to compare categorical variables and proportions, Shapiro-Wilk test to determine normality, Spearman rank-order correlation to determine strength of association between non-normally distributed continuous variables, and log-rank test to compare time to event data. Analysis was performed using IBM SPSS Statistics, v21, IBM, NY, USA, and GraphPad Prism 6, GraphPad Software Inc, USA. Subject characteristics are shown in Table 2. Frequency of hypoglycaemia was: PPD 10.9%, PTG 3.

Yet, medications have the potential for unwanted effects[1] Ther

Yet, medications have the potential for unwanted effects.[1] Therefore, it is important for

healthcare providers to assist consumers or patients in managing their use of medications. Medication management is a complex Adriamycin mw process that involves a range of healthcare providers. Figure 1 illustrates the nine major ‘steps’ identified in the medication management ‘pathway’.[2] In Australia, provision of medication services is complicated by the division of regulatory aspects of healthcare delivery between the Commonwealth (national) Government and state/territory governments. Currently, the Commonwealth Government oversees registration of healthcare practitioners (including scopes E7080 price of practice), subsidy of pharmaceuticals under the Pharmaceuticals Benefits Scheme (PBS) and the implementation of the National Medicines Policy.[3,4] On the other hand, the state/territory governments manage regulatory aspects relevant to drugs and poisons and healthcare providers not licensed under the national

registration of healthcare practitioners (e.g. paramedics, Indigenous health workers).[4,5] The division of responsibilities and funding, including for public health services, between the Commonwealth and state/territory governments further complicates the delivery of healthcare services, including medication services.[4] The medication pathway is further compromised in rural areas, with consumers’ access next to healthcare services restricted due to limited health workforce capacity as well as geographical, professional and social isolation.[4,6,7] This essentially challenges the existing rural healthcare providers to consistently fulfil the ‘steps’ in the medication pathway and to provide the necessary medication support to consumers. This is of concern in rural areas where there is a lack of services offering alternative or adjunct therapy, which could lead to

increased reliance on medication therapy. Rural healthcare also does not provide a favourable environment to comply with key objectives outlined in the National Medicines Policy, specifically (1) timely access to affordable medications, (2) responsible and quality delivery of medication services with best-practice regulatory systems in place and (3) Quality Use of Medicines (QUM), which encompasses judicious, appropriate, safe and efficacious use of medications.[3,4,6,7] The dynamics of rural health have been shown to foster changing or extended clinical roles or skills and differential healthcare models to cope with rural health demands.[6] However, few studies have explored the effect of rural location on the medication pathway in Australia and how rural healthcare providers are coping with the medication needs of consumers or patients. The majority of published studies reviewing rural QUM processes have been limited to individual professions (e.g.

Yet, medications have the potential for unwanted effects[1] Ther

Yet, medications have the potential for unwanted effects.[1] Therefore, it is important for

healthcare providers to assist consumers or patients in managing their use of medications. Medication management is a complex Ibrutinib process that involves a range of healthcare providers. Figure 1 illustrates the nine major ‘steps’ identified in the medication management ‘pathway’.[2] In Australia, provision of medication services is complicated by the division of regulatory aspects of healthcare delivery between the Commonwealth (national) Government and state/territory governments. Currently, the Commonwealth Government oversees registration of healthcare practitioners (including scopes click here of practice), subsidy of pharmaceuticals under the Pharmaceuticals Benefits Scheme (PBS) and the implementation of the National Medicines Policy.[3,4] On the other hand, the state/territory governments manage regulatory aspects relevant to drugs and poisons and healthcare providers not licensed under the national

registration of healthcare practitioners (e.g. paramedics, Indigenous health workers).[4,5] The division of responsibilities and funding, including for public health services, between the Commonwealth and state/territory governments further complicates the delivery of healthcare services, including medication services.[4] The medication pathway is further compromised in rural areas, with consumers’ access ID-8 to healthcare services restricted due to limited health workforce capacity as well as geographical, professional and social isolation.[4,6,7] This essentially challenges the existing rural healthcare providers to consistently fulfil the ‘steps’ in the medication pathway and to provide the necessary medication support to consumers. This is of concern in rural areas where there is a lack of services offering alternative or adjunct therapy, which could lead to

increased reliance on medication therapy. Rural healthcare also does not provide a favourable environment to comply with key objectives outlined in the National Medicines Policy, specifically (1) timely access to affordable medications, (2) responsible and quality delivery of medication services with best-practice regulatory systems in place and (3) Quality Use of Medicines (QUM), which encompasses judicious, appropriate, safe and efficacious use of medications.[3,4,6,7] The dynamics of rural health have been shown to foster changing or extended clinical roles or skills and differential healthcare models to cope with rural health demands.[6] However, few studies have explored the effect of rural location on the medication pathway in Australia and how rural healthcare providers are coping with the medication needs of consumers or patients. The majority of published studies reviewing rural QUM processes have been limited to individual professions (e.g.

A computerized cognitive test battery was undertaken (CogState™,

A computerized cognitive test battery was undertaken (CogState™, Melbourne, Victoria, Australia), which has previously been described in detail [6, 8] and validated in HIV-infected subjects [9]. In brief, all tasks within the battery were adaptations of standard neuropsychological and experimental psychological tests, which assessed a range of cognitive functions. This battery assessed the following domains: detection, identification, monitoring and matched learning (all assessed via speed of test); associate learning and working memory (assessed Idelalisib concentration via accuracy of test); and executive function (assessed via number of errors made

on testing). The battery consisted of tasks in the form of card games. Therefore, subjects

needed only to have an understanding of playing cards, thereby minimizing language and cultural differences among study subjects. Card game instructions were translated into the local language. All study participants HSP cancer completed one full practice test prior to undertaking the study examination to obtain optimal performance at baseline [10]. Statistical analyses were conducted with sas version 9.13 (SAS, Cary, NC) and stata version 10.1 (Statacorp, College Station, TX) and analysis was conducted according to CogState™ recommendations. Reaction times were log10-transformed because of a positive skew of the distribution, and accuracy measures were transformed using arcsine-root transformation. Change scores were calculated for each subject, and these scores standardized according to the within-subject standard deviation (SD). Changes in performance for arms 2 and 3 compared with arm 1 were standardized with a pooled SD, and this was used as the outcome variable in linear regression models to calculate an overall check details effect size for the difference between treatment groups. Composite scores were calculated overall and for the speed and accuracy domains based on the average of standardized scores, and composite changes from baseline scores to weeks 24 and 48 were calculated based on the average of standardized reaction time and accuracy scores. Of 30 subjects enrolled in the

study, 28 completed NC testing at baseline, week 24 and week 48 and were included in this analysis (nine, eight and 11 subjects in arms 1, 2 and 3, respectively). Two subjects who completed baseline NC testing did not attend for follow-up study visits. CD4 lymphocyte count (SD) rose over the 48-week study period from 218 (87) to 342 (145) cells/μL at baseline and week 48, respectively. Other baseline characteristics have previously been described [6]. Of interest, all subjects apart from one had undetectable plasma HIV RNA (<50 HIV-1 RNA copies/mL) at week 48. All statistical results described are unchanged when adjusted for the one subject with detectable plasma HIV RNA at week 48. Overall, improvements in NC function were observed by week 24 and continued to week 48 (Table 1).

, 2009) A close inspection of the PhaR-binding sequences of thes

, 2009). A close inspection of the PhaR-binding sequences of these genes

revealed a very striking similarity among them. The PhaR-binding sequence present in the phaZ promoter is CTGCCATGCAG (located at nucleotides −77 to −67 relative to the initiation codon of phaZ). The one located in the phaC promoter is CTGCATGGCAG (nucleotides −35 to −25 relative to the initiation codon of phaC), and that in the phaR promoter is CTGCAGCCGCAG (located at nucleotides −31 to −20 relative to the initiation codon of phaR). The only difference among these sequences is in the space Proteases inhibitor region. The sequence of the spacer region of the PhaR-binding motif of the phaZ gene is CAT, and those for phaC and phaR are ATG and AGCC, respectively. This is consistent with our finding that the sequences in the two dyad regions of the PhaR-binding motif cannot be changed, but that in the spacer can be substituted by any three or four nucleotides (Fig. 2). Although PhaR can bind to the promoter regions of phaP, phaR, phaZ, and phaC, it regulates these genes differently. PhaR represses the expression of phaP, HSP inhibitor drugs phaR, and phaZ, but not phaC (Chou et al., 2009). The phaZ and phaC genes are located next to each other in an opposite direction and share the same PhaR-binding motif.

However, binding of PhaR to this motif inhibits phaZ expression, but has no suppressive effect on phaC (Chou et al., 2009). This interesting regulatory mechanism is being investigated. We thank Chao-Hung Lee for valuable discussions and critical editing of the manuscript. This study was supported by a grant (NSC96-2311-B-030-001) from the National Science Council, Arachidonate 15-lipoxygenase Taipei, Taiwan. “
“Alarmone Guanosine 5′-diphosphate (or 5′-triphosphate) 3′-diphosphate [(p)ppGpp]

is the key component that globally regulates stringent control in bacteria. There are two homologous enzymes, RelA and SpoT in Escherichia coli, which are responsible for fluctuations in (p)ppGpp concentration inside the cell, whereas there exists only a single RelA/SpoT enzyme in Gram-positive bacteria. We have identified a bifunctional enzyme with (p)ppGpp-hydrolase/synthase activity in Leptospira interrogans. We show that the relLin gene (LA_3085) encodes a protein that fully complements the relA/spoT double mutants in E. coli. The protein functions as a (p)ppGpp degradase as well as a (p)ppGpp synthase when the cells encounter amino acid stress and deprivation of carbon sources. N-terminus HD and RSD domains of relLin (relLinN) were observed to restore growth of double mutants of E. coli. Finally, We demonstrate that purified RelLin and RelLinN show high (p)ppGpp synthesis activity in vitro. Taken together, our results suggest that L. interrogans contain a single Rel-like bifunctional protein, RelLin, which plays an important role in maintaining the basal level of (p)ppGpp in the cell potentially contributing to the regulation of bacterial stress response.

All D:A:D and individual cohort procedures are developed in accor

All D:A:D and individual cohort procedures are developed in accordance with the revised 1975 Helsinki Declaration. We assessed the following individual endpoints in these analyses: Cyclopamine molecular weight MI (including fatal and nonfatal cases); coronary heart disease (CHD; MI plus invasive coronary artery procedure, including coronary artery bypass or angioplasty, or death from other CHD); CVD (CHD plus carotid artery endarterectomy, or stroke); and all-cause mortality. All endpoints are protocol defined, audited for completeness and centrally validated. In the D:A:D study, smoking status is reported as current smoker (yes/no) and ever smoker

(yes/no) at each visit. Dates of stopping or starting smoking are not recorded. Patients were therefore categorized as never smokers, previous smokers, current smokers or smokers who had stopped smoking during D:A:D follow-up. Without dates of stopping or starting cigarette smoking, reasonably accurate times since stopping smoking could only be calculated for those subjects who stopped smoking during the

D:A:D study follow-up period. We calculated time since stopping smoking from the mid-point between the last visit where a subject reported being a current smoker and the selleck chemical first visit where a subject reported being a current nonsmoker. Similarly, subjects who reported

that they started smoking again were taken to do so at the mid-point of the respective visits. Where smoking status was reported to be missing, previous smoking status was carried forward. A sensitivity analysis was also performed omitting all periods of follow-up where smoking status was missing. These analyses were limited to D:A:D patients who ever reported smoking status at enrolment (cohort entry) or during D:A:D follow-up, and had not reported a previous CVD event. Follow-up started at the later of D:A:D cohort entry (enrolment in D:A:D commenced in December 1999) and first reported smoking status, and finished at the earlier of date of death, 6 months after the patient’s last clinic visit or 1 February 2008, whichever occurred first. Celastrol Event rates for each endpoint were calculated for never, previous and current smokers, and smokers who stopped during D:A:D follow-up. Event rates for smokers who stopped during D:A:D follow-up were calculated in annual increments (<1, 1–2, 2–3 and >3 years). Smoking status for individual patients could change during D:A:D follow-up. For example, never smokers may become current smokers and then stop smoking, while previous smokers may restart smoking during follow-up. Crude unadjusted event rates for each smoking status group were calculated.

In contrast, hMLH1 and hMSH2 were absent or had extremely low exp

In contrast, hMLH1 and hMSH2 were absent or had extremely low expression at estrogen levels ranging from 20 to 60 pg/mL, but some cell growth still occurred. Therefore, cells dividing in a low-estrogen environment are more likely Linsitinib to accumulate genetic errors due to low repair activity and may be at high risk for carcinogenesis. Based on these results, Miyamoto et al.[8] suggested that the incidence of growth-induced genetic errors should be low in young women with high estrogen levels and sufficient repair activity of MMR proteins, making carcinogenesis unlikely. In older women with lower estrogen

but an atrophic endometrium, carcinogenesis would also be unlikely because of the absence of cell growth. However, under perimenopausal Alpelisib molecular weight conditions, the carcinogenic risk would

be increased because sufficient estrogen is present to promote cell division, but MMR activity is low. This intermediate status was defined as the cancer window (Fig. 1). The mismatch repair (MMR) system is responsible for repairing base mismatches that arise during DNA replication. Typical MMR proteins include hMLH1, hMSH2, hPMS2, hMSH3 and hMSH6. Genes encoding these proteins are called MMR genes and aberrations in these genes prevent correct repair of mismatched bases, resulting in DNA strands with different lengths. This phenomenon occurs in microsatellite regions of the human genome and is referred to as microsatellite instability (MSI). Microsatellites or short tandem repeats (STR) are repeating sequences of one to five base pairs of DNA, such as CA and CAG. Some STR

occur in regions encoding phosphatase and tensin homolog deleted on chromosome ten (PTEN), a lipid phosphatase that is a tumor suppressor gene; TGF-βR2 and IGF2R, which are associated with inhibition of cell proliferation; K-ras, which is involved in cell proliferation; and BAX, which is related to apoptosis induction. Therefore, MSI is implicated in carcinogenesis.[9] Aberrations in MMR genes are involved in carcinogenesis of type I endometrial cancer. These aberrations are caused by epigenetic changes independent of the DNA sequence, that is, gene inactivation by aberrant hypermethylation of promoter regions. Such inactivation of MMR genes permits accumulation of gene mutations and leads to carcinogenesis. Resveratrol In endometrial cancer, carcinogenesis most frequently involves aberrant methylation of hMLH1 and mutation of hMLH1 is detected in 30% of cases. Mutations of hMLH1 are also found in atypical endometrial hyperplasia, which suggests that hMLH1 is implicated in the early stage of carcinogenesis.[10, 11] Muraki et al.[12] reported aberrant hMLH1 hypermethylation in 40.4% of patients with endometrial cancer and found significantly reduced hMLH1 protein levels in these patients (P < 0.01). However, none of the four cancer-related genes were aberrantly methylated in the normal endometrium. MMR genes are also causative genes in Lynch syndrome (hereditary nonpolyposis colorectal cancer).

The size of DNA fragments ranged from 1030 to 19 937, 1000 to 11 

The size of DNA fragments ranged from 1030 to 19 937, 1000 to 11 247, 521 to 21 735, and 380 to 31 103 bp in

the four phages, φVh1, φVh2, φVh3, and φVh4, respectively. XbaI produced more number of fragments (13, 12, 16, and 18) ranging from 492 to 28 279, 1034 to 11 254, 458 to 11 331, and 224 to 39 618 bp of the four phages, respectively (Fig. 3). The genome size based on PFGE profiles generated with ScaI and XbaI showed little variation (0.8–3.3 kb) with the two enzymes, and the genome size of each phage was calculated as an average of the two profiles. The estimated genome size of the four phages was 85, 58, 64, and 107 kb corresponding to φVh1, φVh2, φVh3, and φVh4, respectively. The phylogenetic analysis of phages based on DraI REA pattern showed distinct nature of phage φVh3, which separated from the cluster of the other three siphoviruses at 63% hierarchical level (Fig. 4a). Similarly, the phylogenetic analysis based on PFGE selleck chemical upon restriction with ScaI and XbaI revealed that the phage φVh3 was distinct and did not cluster with other three siphoviruses as observed in the cluster analysis of DraI REA (Fig. 4b and c). Among the three Ferroptosis inhibitor clinical trial siphoviruses, phage φVh4 was distinct from the other two phages, which branched separately at 56% and 70% hierarchical level in the ScaI and XbaI PFGE dendrograms, respectively. Phages φVh1 and φVh2 showed clustering

at 83% and 86% hierarchical level with ScaI and XbaI, respectively, suggesting their similarity. Vibrio harveyi Vh57 Depsipeptide purchase susceptible to all the four phages was successfully transformed with the plasmid DNA (pHSG396). The transformants harboring the plasmid produced blue colonies on PYSS agar supplemented with chloramphenicol, Xgal, and

IPTG. The transductants obtained after infection of plasmid transformed donor strain with the four phages grew on PYSS medium supplemented with chloramphenicol producing blue colonies as they acquired the plasmid PHSG 396 DNA. The frequency of transduction of four phages ranged from 4.1 × 10−7 to 2 × 10−9 PFU−1 (Table 1). So far, 227 tailed phages infecting Vibrio spp. have been described, among which 67 belonged to the family Siphoviridae (Ackermann, 2007). In this study, three phages (φVh1, φVh2, and φVh4) with a long noncontractile tail (130–329 nm long) and an isometric head (approximately 60–115 nm in diameter) belonged to the family Siphoviridae and resemble the phages described earlier (Pasharawipas et al., 2005; Vinod et al., 2006; Shivu et al., 2007). One phage, φVh3, belonged to the family Podoviridae according to criteria of head, tail, and genetic material (Ackermann, 2001). According to Ackermann, capsid and tail size of tailed phages range from 30 to 160 and 10 to 800 nm, respectively (Ackermann, 2005). Reports on the isolation of bacteriophages belonging to the family Podoviridae from the aquaculture ecosystems are scanty. A member of this group infecting V.

However, the impact attributable to HIV itself may still be impor

However, the impact attributable to HIV itself may still be important. The CNS HIV Anti-Retroviral Therapy Effects Research (CHARTER) study found a lower CD4 cell count nadir to be a significant risk factor for neuropathy [15]. In the HIV Outpatient Study (HOPS) cohort, low nadir CD4 cell count and high plasma HIV RNA at first visit were a nearly equivalent or stronger predictor of developing neuropathy than use of ARV

medications, with the exception of higher dose d4T [16]. Our study results are consistent with pre-HAART data and demonstrate that peripheral nerve damage is seen at lower CD4 cell counts among individuals free of clinical neuropathy signs and/or symptoms. The findings of this study are also consistent with other reports that have identified age and height as significant predictors of neuropathy risk [15, 17, 18]. High ENFDs are seen in young people [19] and remodelling and ‘pruning’ of epidermal nerves may be part of BMS-354825 cost the aging process. The aetiology of HIV-SN even in the absence of ARV medications may include important contributions from

mitochondrial dysfunction. Recently, mtDNA damage was demonstrated to be more pronounced in the distal mitochondria of long axons from post mortem patients who CHIR-99021 cell line died with HIV-SN, consistent with the length-dependent nature of this neuropathy [20]. Furthermore, terminal nerve endings in skin from HIV-infected patients have demonstrated abnormal mitochondrial accumulations [21]. Depletion of PBMC mtDNA and OXPHOS enzyme activities has been observed in ARV-naïve subjects, suggesting that HIV in the absence of ARV medications causes mitochondrial dysfunction [22, 23]. Older potentially mitochondrial-toxic NRTIs [d4T and didanosine (ddI)] are still used as components of ARV regimens enough in developing countries. Pre-existing mitochondrial dysfunction related to HIV may increase the risk of neuropathy when such drugs are used. Adequate energy production is necessary for normal metabolism; thus, our initial expectation was that lower

ENFD, as a predictor of peripheral nerve damage, would be associated with lower OXPHOS enzyme activities. However, our study found that OXPHOS CI and CIV activity levels increased, rather than decreased, as ENFD decreased. We speculate that such increases in PBMC OXPHOS enzyme activities among ARV-naïve patients with lower ENFD may represent a general increase in cellular energy requirements secondary to increases in inflammatory tendencies mediated by HIV. In vitro, HIV infection has been reported to increase CIV activity in HIV-infected T cells [24]. In another tissue source, we have reported increases in ATP level within adipocytes from ARV-naïve subjects compared with HIV-seronegative controls [25]. Our study has several important limitations. Its applicability is limited to subjects of Thai descent and to those free of clinically defined neuropathy.

, 2008) This could well constitute a mechanism of expansion of t

, 2008). This could well constitute a mechanism of expansion of the periodontal pocket epithelium, which is a histopathological

feature of periodontitis. It is now well established that P. gingivalis is not an aggressor of the inflammatory response, but rather an opportunist that can cross-talk with the host and subvert its defence mechanisms. Using this strategy, P. gingivalis prolongs its survival and becomes established in the periodontal pocket (Hajishengallis et al., 2011). It preferentially deregulates innate immunity, which may in turn disable adaptive immunity (Hajishengallis, 2009; Pathirana et al., 2010). Important representative examples of these abilities are its capacity to degrade human defensins www.selleckchem.com/products/nu7441.html (Carlisle et al., 2009), its resistance to oxidative www.selleckchem.com/products/sotrastaurin-aeb071.html burst-killing by polymorphonuclear neutrophils (PMNs) (Mydel et al., 2006) and its ability to inhibit ‘at will’ the production of crucial proinflammatory cytokines (Bostanci et al., 2007a, b). Although P. gingivalis has the capacity to stimulate interleukin (IL)-8 production by epithelial cells (Sandros et al., 2000; Asai et al., 2001; Kusumoto et al., 2004), it can also inhibit IL-8 production, resulting in hindered PMN chemotaxis, a phenomenon known as ‘chemokine paralysis’ (Darveau et al., 1998). Porphyromonas gingivalis thereby incapacitates the first line of

defence in the periodontal tissues. Moreover, by inhibiting IL-12

production by macrophages, it prevents cytotoxic T-cell activation and therefore bacterial clearance (Hajishengallis et al., 2007). Accordingly, by inhibiting interferon (IFN)-γ production by T cells, it inhibits macrophage bacteriocidal activity Oxalosuccinic acid and hence bacterial clearance (Pulendran et al., 2001; Hajishengallis et al., 2007). A special relationship is also revealed between P. gingivalis and the complement system, as it can suppress its activation, that is by degradation of C3 and capturing of C4b-binging protein, but also by synergizing with C5a via exploiting toll-like receptor (TLR)-2 signalling (Wang et al., 2010). A further interesting point is that whole viable P. gingivalis is differentially sensed by the host, compared with its released virulence factors, with the potential to activate distinctive intracellular pathways (Pathirana et al., 2010), or differential cytokine production (Zhou et al., 2005). As an opportunistic pathogen, it is not surprising that P. gingivalis possesses a number of virulence factors. These are molecules that can elicit deleterious effects on host cells, essentially the survival ‘weapons’ of P. gingivalis. The main virulence factors discussed here are LPS, capsular polysaccharide (CPS), fimbriae and gingipains. Like all Gram-negative bacterial species, P.