9 5.0-9.8) log10 copies/mL], and the serum alanine aminotransferase Tofacitinib Citrate clinical (ALT) was 174.6 �� 7.78 IU/L [median: 113 (99-567) IU/L]. All patients received telbivudine 600 mg/day for 48 weeks. The serum ALT level, HBsAg, HBeAg, anti-HBc, anti-HBe, anti-HBs and HBV DNA were tested every 12 weeks during the telbivudine therapy. Healthy donors (n = 10) were included as controls. Flow cytometry Peripheral blood mononuclear cells (PBMC) were isolated from ethylenediaminetetraacetic acid (EDTA) anticoagulated blood samples on a Ficoll-Histopaque density gradient. After isolation, cells were washed twice in phosphate-buffered saline (PBS) and studied immediately. CD127, CD8, CD27 and CD45RA expression on the PBMC was detected by direct staining. CD127 expression on HBV-specific CD8+ T cells was performed as described previously [10].

Briefly, PBMC were stained with surface PC5-anti-CD8 (BD Pharmingen, San Diego, CA, USA) and pentamer+ CD8 T cells were detected by staining with phycoerythrin (PE)-labelled pentameric peptide-HLA2 complex (ProImmune, Oxford, UK) containing HBV Core 18-27 (FLPSDFFPSV) and HBV Core 18-27 (FLPSDFFPSI). Gated on CD8 T cells, CD127 expression on HBV-specific CD8 T cells was analyzed by fluorescein isothiocynate (FITC)-anti-CD127 and PE-labelled pentamers. Cells were washed three times with PBS, and 1 �� 106 events in the lymphogate were collected by flow cytometry (EPICSXL; Coulter, Fullerton, CA, USA). Data were analyzed using CellQuest software (Coulter). Statistical analysis The Wilcoxon matched pairs test and the Mann-Whitney test of SPSS version 12.

0 were used to assess differences among groups. Spearman correlation analysis was performed between CD127 expression and serum HBV DNA and HBeAg levels. P-values less than 0.05 were considered statistically significant. Results CD127 expression on memory CD8 T cells was reduced in patients with chronic hepatitis B Ex vivo expression of CD127 by different CD8 T lymphocyte subsets taken from patients with CHB were checked by flow cytometry. As indicated in Fig. Fig.1a,1a, naive CD8 T cells (CD45RA+CD27+) from CHB patients showed a high percentage of CD127+ cells, as did the cells from healthy controls. When the expression of CD127 was examined in memory CD8 T cells (CD45RA-CD27+) and effector CD8 T cells (CD45-RACD27-), we found significant decrease of CD127 expression in CHB patients compared with healthy controls.

Terminally differentiated effector CD8 T cells (CD45RA+CD27-) from both CHB patients and healthy controls expressed little CD127, as indicated in Fig. Fig.1b1b. Figure 1 Ex vivo expression of CD127 by memory GSK-3 CD8 T cells taken from chronic hepatitis B (CHB) patients. (a) CD127 expression by CD27+CD45RA+ naive CD8 T cells. Results are shown for one healthy control and two CHB patients. (b) Proportion of CD127+ lymphocyte …

008 to 1.0 ��g/ml for the frozen sections) in 50 mM Tris (pH 7.5) at 37��C for 30 min in a humidified chamber. Subsequently, proteinase things K was inactivated at 97��C for 10 min, and then the sections were rinsed with distilled water, dehydrated in 99.5% ethanol, and air dried. Primers and probes for PCR-ISH and RT-PCR-ISH. The primers used to amplify the S and X regions of HBV and the 5�� untranslated region (5��-UTR) of HCV as well as the corresponding probes are listed in Table Table2.2. We created a digoxigenin (DIG)-dUTP tail at the 3�� end of the 5��-DIG probe using a DNA tailing kit (Roche, Basel, Switzerland). TABLE 2. Primers and probes for PCR-ISH and RT-PCR PCR-ISH for detecting HBV DNA. PCR was performed by using one of two sets of antisense and sense primers complementary to the sequences located in the S and X regions of HBV.

The PCR mixture contained 10 mM Tris-HCl (pH 8.3), 50 mM KCl, 3.0 mM MgCl2, 0.8 mM each primer, 197 mM deoxynucleoside triphosphates (dNTPs), and 10 U/50 ��l Taq DNA polymerase (AmpliTaq Gold; Applied Biosystems). The tissue slides were warmed to 70��C, and 50 ��l of the PCR mixture was overlaid onto the proteinase K-treated tissue specimens. An Ampli cover disc with Ampli cover clips (Applied Biosystems) was attached to each specimen. The slides were placed in the GeneAmp in situ PCR system 1000 unit at 70��C. PCR was performed at 95��C for 10 min, followed by 35 to 55 cycles at 95��C for 30 s and 60��C for 2 min and a final extension at 72��C for 10 min. Immediately after the PCR, the slides were fixed in 4% paraformaldehyde in phosphate-buffered saline (PBS) for 10 min at 37��C, washed in 2�� SSC (1�� SSC is 0.

15 M NaCl plus 0.015 M sodium citrate) for 2 min, rinsed with distilled water for 2 min, dehydrated in 99.5% ethanol for 1 min, and then air dried. ISH was performed by mixing the DIG-labeled probe (final concentration, 100 ng/ml) with 65 ��l of hybridization buffer (50% deionized formamide, 4�� SSC, 1�� Denhardt’s solution [0.2% bovine serum albumin BSA, 0.2% polyvinyl pyrrolidone, 0.2% Ficoll 400], 100 ��g/ml denatured salmon sperm DNA, 100 ��g/ml yeast RNA, and 1 mM EDTA) and then adding the mixture to each section, heating to 97��C for 10 min, and cooling to 37��C in decrements of 1��C/min (27). Hybridization was carried out overnight at 37��C. Stringency washes were conducted with the following: 2�� SSC twice for 10 min at 37��C, 0.

03�� SSC for 10 min at 50��C, 0.1% Triton X-100 in TBS (0.1 M Tris [pH 7.5], 0.1 M NaCl) for 10 min at room temperature, and TBS for 5 min at room temperature. After incubation in blocking reagent (0.1 M Tris [pH 7.5], 0.1 M NaCl, 10% sheep serum, 3% BSA) at room temperature for Carfilzomib 15 min, the slides were covered with 100 ��l anti-DIG antibody conjugated with alkaline phosphatase (Roche) and diluted at 1:900 with 1% BSA in TBS at 37��C for 60 min.

For example, experiences of discrimination are associated with negative affect (e.g., Brondolo et al., 2008) and free overnight delivery with smoking (e.g., Landrine & Klonoff, 2000). Given this, one might argue that the discrimination�Csmoking relation might be mediated by psychological distress. However, the analyses reported here show no relation of psychological distress and smoking for Blacks and Hispanics. It may be that the facets of distress captured by the K6��s focus on overall psychological distress are separate and distinct from those aroused by experiences of discrimination (for an example of specific types of affect having different effects on substance use in the context of discrimination, see Gibbons et al., 2010).

Future research is needed to address the role of sociocultural aspects of race, including discrimination, in the relation of psychological distress to smoking behavior. Finally, the findings about the relation between psychological distress and smoking behavior raise interesting questions about the potential nature of race and ethnic differences in smoking cessation. Success at quitting smoking may differ as a function of race and ethnicity, with Blacks being less likely to maintain abstinence (King et al., 2004; Messer, Trinidad, Al-Delaimy, & Pierce, 2008). Understanding factors contributing to that relationship potentially have implications for how we design targeted intervention programs. Negative affect is associated with smoking relapse (Shiffman & Waters, 2004); the findings concerning differences in the relation of psychological distress to smoking suggest that research examining differences by race in triggers of relapse should be conducted.

Limitations There are, of course, limitations to the study, which should be addressed. First, it is important to note that the study is cross-sectional, so the findings should be properly interpreted as associations between distress and smoking and differences in association by race rather than as patterns of causal relations. Second, it is important to note that the K6 measure is a measure of overall psychological distress. There are specific dimensions of negative affect, which are not well assessed by the measure (e.g., stress, anger; see Collins & Lepore, 2009; Webb & Carey, 2008). Future research should examine a broader spectrum of distress and affective states in relation to smoking status.

Finally, although the study is designed as a population-representative sample, the nature of survey design is such that there may be elements of the population who are not well represented (e.g., individuals without landline telephones, including those with cell phones and low SES individuals) and the point estimates in the survey may not fully mesh with those of other population AV-951 representative reports (e.g.

This resulted in increased costs for chemotherapy administration in the 5-FU/LV arm compared with the capecitabine treatment arm (��5151 and ��419, respectively). Thus, considering both drugs and their administration, chemotherapy costs are lower by ��3253 (57% lower) for capecitabine vs 5-FU/LV. Figure 1 Number of treatment visits for chemotherapy these administration or AEs with capecitabine vs 5-FU/LV. Cost of managing AEs The improved safety profile with capecitabine compared with 5-FU/LV was reflected in the need for fewer costly medications for the management of treatment-related AEs in the capecitabine treatment arm compared with 5-FU/LV (Table 2). In particular, capecitabine reduced the need for the more expensive drugs, such as fluconazole for stomatitis, 5-HT3 antagonists for nausea/vomiting and cytokines for neutropenia.

Overall, the mean cost of medication for management of AEs was lower in the capecitabine arm compared with the 5-FU/LV arm (��86 and ��345, respectively). Table 2 Medications used for management of treatment-related adverse events A similar mean number of physician visits due to AEs were seen in each treatment arm (1.93 and 1.92 for capecitabine and i.v. 5-FU/LV, respectively). However, there were 16% fewer AE-related hospital admissions and 15% fewer days in hospital in the capecitabine treatment arm vs the i.v. 5-FU/LV arm (10.6 and 12.8 admissions, respectively, and 113 vs 130 days, respectively; Figure 2). The mean cost of hospitalisations was consequently lower with capecitabine than with 5-FU/LV (��399 vs ��459), although the cost of physician consultations was slightly increased with capecitabine compared with 5-FU/LV (��154 vs ��145).

In accordance with these findings, the projected ambulance costs would be reduced in the capecitabine group compared with the 5-FU/LV group (��38 vs ��126). Figure 2 Hospital admissions for AEs. Societal costs for time and travel The projected mean number of hours per patient required for travel were lower in the capecitabine group compared with the 5-FU/LV group (27 and 125h, respectively) and the mean costs for travel time were therefore reduced in the capecitabine group (��320 compared with ��1503 in the 5-FU/LV group). Similarly, the mean travel cost per patient was reduced with capecitabine compared with 5-FU/LV (��62 and ��196, respectively).

Total costs Direct costs during the treatment period have been grouped into six components, as illustrated in Table 3. The major drivers for the cost analysis are the cost of the chemotherapy drugs and the cost of administration of treatment. The additional ��4732 required Drug_discovery for i.v. therapy is more than three times the additional acquisition cost of capecitabine. With respect to the management of AEs, the most notable difference was the lower cost of medication used for treating AEs in the capecitabine arm (��86 compared with ��345 in the 5-FU/LV arm).

A: Isolated colonic lamina propria macrophages from the large intestine were incubated with or without heat-killed Streptococcus sp. for 16 hours. mRNA of cells from Mgl1+/+ and … Discussion The hallmark of inflammatory bowel diseases, www.selleckchem.com/products/AZD2281(Olaparib).html including Crohn��s disease and ulcerative colitis, is abnormal inflammation of the gastrointestinal tract, but the pathogenesis has not been fully elucidated. In the present study, Mgl1-deficient mice exhibited a more severe inflammation than wild-type mice in an experimental model for ulcerative colitis. The mechanistic basis for this difference was determined to be a change in cytokine production in response to intestinal commensal bacteria. The predominant portion of cells expressing MGL1 in colonic lamina propria were found to be macrophages, and these cells were shown to produce IL-10 in response to the bacteria.

IL-10 was previously considered a crucial cytokine for the maintenance of intestinal homeostasis because IL-10-deficient mice spontaneously developed colitis.5 The present study clearly shows that lamina propria macrophages lacking Mgl1 produced less IL-10 than these cells expressing MGL1. IL-10 produced by a variety of cells, such as macrophages, DCs, and T cells, plays an important role in the pathogenesis of colitis. In macrophage-depleted mice, DSS-induced colitis was more severe, and IL-10 mRNA from the whole colon of these mice was decreased compared with sham-treated mice, indicating that colonic macrophages secrete IL-10 during colonic inflammation.29 However, the most important target of IL-10 remains unclear.

IL-10 is likely to influence the functions of a wide range of immune cell populations by suppressing pro-inflammatory responses.29 For example, IL-10 is known to suppress production of IL-12, tumor necrosis factor-��, and reactive oxygen species by macrophages and DCs. It also inhibits Th1 and Th2 responses, which aggravate pathogenic inflammation. Colonic epithelial cells are not likely to act as the target of IL-10. IL-10 has been shown to inhibit MHC class II expression on epithelial cell lines, but it does not affect the chemokine secretion responsible for the recruitment of neutrophils and monocytes to injured sites.30,31 By immunohistochemical analysis, MGL1-expressing cells were observed in the lamina propria and in the submucosa, where many other types of immune cells were also observed.

After the induction of colitis, cells expressing MGL1 were absent from this area. Although it is possible that cells expressing MGL1 migrated to other regions, it is likely that MGL1 expression was down-modulated on CD11b+cells, considering that CD11b+ cells with similar morphology were present in this ulcerated region. Furthermore, when isolated lamina propria macrophages were exposed to heat-killed Batimastat Streptococcus sp., these cells significantly reduced the cell surface expression of MGL1, as indicated by the binding of monoclonal antibody LOM-8.

Similarly, our data show that LPS treatment in the colon causes severe inflammation in the small intestine remotely, while it induces proinflammatory cytokine production in the colon without causing adverse effects on the colonic mucosa (Figs. 1 and and2).2). Regarding the small intestinal inflammation remotely www.selleckchem.com/products/mek162.html induced by colonic LPS, we speculate that lamina propria cells in the colon might respond to colonic LPS, or epithelial cells in the colon could be able to sense luminal LPS, to induce inflammatory mediators, which will trigger subsequent inflammatory responses in the small intestine. In answer to question 2, various examples of the protective mechanism against LPS can be proposed. Secretory IgA antibody in the intestine serves as an external barrier to neutralize LPS in the intestine (8).

In addition, the colonic epithelium is rich in mucin-producing goblet cells, and the mucus layer can prevent LPS attachment to the mucosal surface in the colon (21). Although transmural passage of LPS was suggested to be almost imperceptible in the normal colon (23), LPS can be absorbed at a molecular level by a specific cellular transporter, the chylomicron, in the intestinal epithelial cells and, thereby, can induce inflammatory responses (13). In this case, however, immune-suppressive Treg cells and an anti-inflammatory cytokine, such as IL-10, can engage in modulating inflammatory responses (9�C11). Moreover, TLR-inhibitory molecules [e.g.

, Toll-interacting protein (TOLLIP), IL-1 receptor-associated kinase (IRAK-M), single immunoglobulin IL-1 receptor-related protein (SIGIRR), splice variant of myeloid differentiation factor 88 (MyD88s), and TIR domain-containing adaptor-inducing Cilengitide IFN-�� (TRIF)] are strongly expressed or can be upregulated by inflammatory responses in intestinal epithelial cells and, subsequently, can disrupt a prolonged inflammatory response (5). Taken together, although colonic LPS is able to elicit inflammatory responses initially, these protective mechanisms may allow the intestine to contain the inflammatory response. Although we appreciate that a clear answer is not straightforward, thanks to some of these protective mechanisms, mice treated with colonic LPS could recover from the intestinal inflammation. This speculation can be supported by our findings that 1) intestinal inflammation was severe in IL-10?/? mice, and they failed to recover (Fig. 4), and 2) T cell-depleted Rag-1?/? mice could not recover from LPS-induced intestinal inflammation (Fig. 5). We, however, acknowledge that the exact mechanism by which LPS in the colon can induce small intestinal inflammation remotely but does not damage the colonic epithelium locally is still not clear.

4B). Together these results show that at the highest dose of meprins, the decreased abilities of AIEC bacteria to adhere to and invade intestinal epithelial cells were not Trichostatin A (TSA) due to degradation of LF82 OMPs or flagella. Figure 4 Proteolytic activity of meprins �� and �� on AIEC LF82 outer membrane proteins and flagellin. Meprins �� and �� induce proteolytic cleavage of AIEC LF82 type 1 pili Experiments performed in vitro with cultured intestinal epithelial cells, ex vivo with human isolated enterocytes from CD patients, or in vivo using transgenic mice expressing the human CEACAM6 receptors showed that type 1 pili play a key role in the ability of AIEC bacteria to adhere to and invade intestinal epithelial cells [12], [13], [15].

We investigated whether the decrease in the abilities of AIEC bacteria to adhere to and invade epithelial intestinal cells observed after pretreatment of bacteria with meprin �� or meprin �� could be the result of proteolytic degradation of type 1 pili by these proteases. A dose-dependent proteolytic degradation of FimA, the major subunit of type 1 pili, was observed after treatment of AIEC LF82 purified type 1 pili with meprins �� and �� (Fig. 5A). Treatment of LF82 purified type 1 pili with 100 ��g/ml of meprin �� or meprin �� induced a strong decrease in the FimA band observed on SDS-PAGE compared to untreated type 1 pili (89% for meprin �� and 72% for meprin ��). We also analyzed the proteolytic activity of meprins on type 1 pili present on the surface of whole bacteria.

The amount of FimA subunit relative to that of the inner membrane protein Lep was determined by Western blot after treatment of LF82 bacteria with active or heat-inactivated meprin �� or ��. We observed 58% and 34% decreased amounts of FimA after treatment of the bacteria with active meprins �� and ��, respectively compared to those of untreated bacteria (Fig. 5B). In contrast, when bacteria were treated with heat-inactivated meprins the amount of FimA was unchanged. The degradation products of purified AIEC LF82 type 1 pili following meprin treatment were analyzed by mass spectrometry. Treatment of purified LF82 type 1 pili with 100 ��g/ml of active meprins �� and ��, compared to heat inactivated meprins, modified the mass spectrometry profile of type 1 pili (Fig. 5C and 5D). A decrease in the intensity of the base peak of spectrum corresponding to the protonated form ([M + H]+) of major analyte detected between 16259 and 16267 m/z was observed after treatment with Entinostat meprins. This was no longer observed with heat inactivated meprins. The same observation was made with the doubly protonated form ([M + 2H]2+) of this analyte, detected between 8130 and 8134 m/z after treatment with active meprins.

Given a two-sided alpha = .05 chi-square test adjusted for clustering within high schools with an intracluster correlation of .02, a total sample size of 40 click here high schools each with an average enrollment of 150 male ST users was estimated to be needed to provide 90% power to detect a significant difference in quitting of 15% in intervention high schools to 5% in no-intervention high schools. For a high school to be eligible for inclusion in the study, it had to be located in one of 29 totally rural CA counties (a population density of 250 persons or less per square mile and no township of >50,000 persons; California State Rural Health Association, 2009). In these rural counties, there were 217 eligible high schools.

Student eligibility criteria were: male enrolled in a study high school, parental consent if 17 years of age and younger, student-signed informed assent, and reported tobacco use within the past 30 days to be considered a tobacco user. Sample selection, recruitment, informed consent, and randomization Study investigators contacted the tobacco control coordinator in the County Office of Education (COE) in each of the 29 totally rural counties (of 58 total) in CA to explain the study and to gain agreement for collaboration to recruit county high schools. Twenty-one (72.4%) of 29 counties agreed to work with study investigators to gain permission from school district superintendents and high school principals in their county by writing a letter of study support. High schools were randomly selected from a list of public high schools in these counties from the California Public Schools Directory (1993) and recruited over 4 years.

In brief, from 2000 to 2004, 41 high schools were enrolled in the study: 8 in Year 1, 15 in Year 2, 10 in Year 3, and 8 in Year 4. Investigators contacted high school principals to explain the study and gain consent for their high schools�� participation the following Fall. As a participation incentive, investigators donated $150 to each participating high school supporting their graduation dance. Schools declining to participate were replaced with another randomly selected school. The high school principal��s cover letter and study consent form were included in the students�� fall registration packets. The cover letter explained the purpose, methods, benefits, and risks of the study and provided a toll-free telephone number for parents who had questions for a study investigator.

Year 1 of the study used active parent consent, but subsequent years used passive parent consent (i.e., opt out) as detailed elsewhere (Gansky et al., 2008). Student participants provided written assent. Participating high schools, stratified on size of school and Carfilzomib enrollment year, were randomly assigned to either the intervention or the no-intervention group. Questionnaire assessment Baseline For each high school, a local person (either staff from the COE or the participating high school, i.e.

Table 1 Characteristics of included studies. TDF received approval for the treatment of HIV infection from the United States Food and Drug Administration (FDA) in October 2001 and from the Brefeldin A ATPase European Medicines Agency in February 2002. (FDA approval for the treatment of chronic HBV infection was granted in August 2008.) The first reports of the use of TDF in treating HBV infection were presented in 2002. Web of Science, Embase and Medline were searched, including all years. Conference abstracts from The Liver Meeting (American Association for the Study of Liver Diseases), The International Liver Congress (European Association for the Study of the Liver) and the Conference on Retroviruses and Opportunistic Infections were searched for the years 2002�C2010.

To search databases, a combination of key terms was used including ��hepatitis��, ��HIV��, and ��tenofovir��, limited to articles with human subjects and written in English (Appendix S1). Conference abstracts were searched online or by hand. Other publications that were discovered from the reference lists in publications reviewed were also included. Data Collection Studies were screened initially by title and then data was collected by HP from the full article of all published studies and from conference posters, or conference abstracts if posters were not available. Some studies met the eligibility criteria except that the published report did not include data on the number with undetectable HBV viral load at one year, or information on prior or concomitant drug exposure.

The authors of these studies were contacted by email and asked to provide additional data if available. Additional, unpublished data was obtained from the authors of 11 of the 23 sources included (Table 1). The authors of one conference report provided an article that superseded the conference report and which had been accepted and published online but that had not been discovered in the search [13]. Data collected consisted of type of study, source of study funding, number of HBV/HIV coinfected participants, number HBeAg positive at study entry, prior 3TC/FTC exposure, drug regimens used during study period, length of follow-up, type of HBV viral load test used and lower limit of detection, numbers tested for HBV viral load at yearly intervals, and numbers with undetectable Dacomitinib HBV viral load at yearly intervals. To maximise power and in the absence of any evidence suggesting a difference in effect on HBV between 3TC and FTC, exposure to these two were grouped together. Results were stratified by treatment into four groups.

Therefore, repeated exposure of tumour cells to photodynamic therapy does not seem to result in loss of DNA mismatch Verdinexor (KPT-335)? repair, and loss of mismatch repair, in turn, does not seem to contribute to resistance to photodynamic therapy. Our results suggest recommending photodynamic therapy as a strategy for circumventing resistance due to loss of DNA mismatch repair. British Journal of Cancer (2002) 86, 1130�C1135. DOI: 10.1038/sj/bjc/6600218 www.bjcancer.com ? 2002 Cancer Research UK Keywords: photodynamic therapy, DNA mismatch repair, drug resistance, m-THPC DNA mismatch repair (MMR) proteins repair mispaired DNA bases and have an important role in maintaining the integrity of the genome (Modrich, 1997). Loss of MMR is the genetic basis for the hereditary nonpolyposis colon cancer syndrome and is a common finding in a variety of sporadic human tumours.

Recent studies have documented that loss of MMR is an important mechanism of resistance to a variety of clinically important drugs, including cisplatin (Aebi et al, 1996; Fink et al, 1996) and the topoisomerase II poisons (Fedier et al, 2001). This is due, in part, to the fact that the MMR system can recognise and bind to various types of adducts in DNA. In addition, the genomic instability that accompanies loss of MMR can increase the rate of mutation in coding or regulatory sequences of other genes whose products may play central roles in determining tumour cell sensitivity to drugs. Loss of MMR has been reported in tumour cell lines selected by repeated treatments for resistance to cisplatin, methylating agents and doxorubicin (Aebi et al, 1996; Brown et al, 1997).

Although the reports are controversial there is some evidence that MMR-deficient cells are also resistant to ionising radiation (Fritzell et al, 1997; Xu et al, 2001). The development of drug resistance during chemotherapy of initially chemosensitive tumours is a frequent problem in clinical oncology, since it may lead to tumour progression and finally to the death of the patient. Thus, finding new treatment modalities effective against MMR-deficient tumour cells is of the utmost clinical importance. Photodynamic therapy (PDT) is being evaluated as an alternative treatment option for chemotherapy-resistant tumours (Canti et al, 1995). PDT uses laser light of appropriate wavelength and energy to activate a systemically applied photosensitiser that concentrates preferentially in malignant tissues. A photochemical reaction ensues, leading Anacetrapib to selective tumour necrosis (Dougherty et al, 1975). 5,10,15,20-meta-tetra(hydroxyphenyl)chlorin (m-THPC) is a neutral lipophilic second-generation photosensitiser with an absorption maximum at 652nm.