0) preheated to 80°C, maintaining this temperature and keeping sections in this solution for 10 min in a microwave pressure cooker. After allowing the sections to cool to room temperature, the slides were rinsed in PBS (pH 7.4). Endogenous peroxidase activity was blocked by incubation of the tissue samples for 10 min in 3% hydrogen peroxide. Samples were incubated for 45 min with the primary antibodies at room temperature in a moisture chamber. VEGF determination and analysis Samples were incubated with mouse anti-VEGF monoclonal antibody (1:100) INCB018424 cost (Abcam, Cambridge

MA, USA) in BSA 1% in PBS for 45 min. After washing with PBS, binding of the primary antibodies was revealed by incubation for 20 min with LSAB+ System Link (DAKO, selleck kinase inhibitor Carpinteria, CA, USA) and LSAB+ HRP, (Streptavidin HRP kit, DAKO). The slides were rinsed with PBS and exposed to diaminobenzidine for 5 min. After washing with PBS and counter-staining with hematoxylin, the slides were dehydrated by graduated alcohols and xylol, and mounted with Poly-mount. Numerical proportions of stained cells were established by analyzing 10 high-power fields (400×) in each section.

Only cytoplasmic staining was considered positive. Intensity was graded on a semi-quantitative scale from 0–3. Graduation of expression was considered negative if fewer than 5% of cells were stained. Determination of vascular density The samples were incubated for 45 min with mouse anti-CD34 monoclonal antibody (1:200) Celastrol (Biocare Medical, Concord, CA, USA) as a marker for vascular endothelial cells. Three separated, highly vascularized areas (“”hot spots”"), KU-60019 price previously identified in high-power fields (100×, then 400×), were analyzed by two pathologists by means of optic microscopy without previous knowledge of hCG determinations. Any immunostained vessel clearly separated from adjacent vessels with no muscular wall and within the optic field was considered a neovascularization vessel.

Vascular density (VD) was considered as the average of the three evaluated zones. Statistical analysis For descriptive purposes, continuous variables were summarized as arithmetic means, medians, and standard deviations (SDs), while categorical variables were expressed as proportions and confidence intervals (CIs). Inferential comparisons were carried out using the Student t or the Mann-Whitney U test, according to data distribution determined by the Kolmogorov-Smirnov test. Chi square or Fisher exact test was used to assess significance between categorical variables. Statistically significant and borderline-significant variables (p < 0.1) were included in the multivariate logistic regression analysis. Overall survival time was measured from day of surgery to date of death or last follow-up visit and analyzed with the Kaplan-Meier method, and comparisons among sub-groups were performed with the log-rank test. For survival curve analysis, all variables were dichotomized.

9) 45 (80.4) 32 (91.4)   0.31 72 (88.9) 52 (86.7) 39 (76.5) 0.69 0.06 Selleck BAY 11-7082    G eFT508 datasheet carrier 31 (17.1) 11 (19.6) 3 (8.6) 0.67   9 (11.1) 8 (13.3) 12 (23.5)     MMP-9                        A carrier 78 (42.6) 19 (33.3) 15 (41.7) 0.21 0.92 25 (30.5) 22 (36.1) 22 (43.1) 0.48 0.14    G/G 105 (57.4)

38 (66.7) 21 (58.3)     57 (69.5) 39 (63.9) 29 (56.9)     TIMP-1                       ♀ T carrier ♂ T 148 (80.9) 41 (73.2) 29 (80.6) 0.22 0.97 46 (56.8) 31 (50.8) 26 (51.0) 0.48 0.51    C/C C 35 (19.1) 15 (26.8) 7 (19.4)     35 (43.2) 30 (49.2) 25 (49.0)     TIMP-2                        C carrier 54 (30.2) 17 (32.1) 10 (28.6) 0.79 0.85 27 (33.3) 20 (32.3) 13 (25.5) 0.89 0.34    G/G 125 (69.8) 36 (67.9) 25 (71.4)     54 (66.7) 42 (67.7) 38 (74.5)     Abbreviations: DU, duodenal ulcer; GU, gastric ulcer. The p value was determined by Fisher’s exact test or χ2 test. a indicated significance with p < 0.05 of such parameter between gastritis and duodenal ulcer; b between gastritis and gastric ulcer. Genotype distribution of SNP in cases and control was in Hardy-Weinberg equilibrium (p < 0.05). There was a higher rate of MMP-3 6A6A genotype in patients with duodenal ulcers than in patients with gastritis (87.7% vs. 74.9%, p < 0.05). H. pylori-infected subjects with the MMP-3 6A6A genotype had a 2.4-fold (95% CI: 1.02-5.66)

increased risk of duodenal ulcer in females compared to those with the 5A carrier. Because www.selleckchem.com/products/ulixertinib-bvd-523-vrt752271.html TIMP-1 genotypes modulated MMP-3 activity, it was further tested whether the MMP-3-1612/TIMP-1372 Combined genotypes contributed to increased

risk of duodenal ulcers in females. The combined MMP-3/TIMP-1 genotype as 6A6A/CC had a 3.6-fold (p < 0.05) increased risk of duodenal ulcer in H. pylori-infected female (Table 4). Table 4 Risks of combined MMP-3/TIMP-1 genotype for developing duodenal ulcer in females   Gastritis Duodenal ulcer OR (95% CI) P MMP-3 -1612 - TIMP-1 372 n (%) n (%)        5A carrier - T carrier 39 (88.6) 5 (11.4) 1 -    5A carrier - C/C 7 (77.8) 2 (22.2) 2.23 (0.36 - 13.85) 0.59 6A/6A - T carrier 109 (75.2) 36 (24.8) 2.58 (0.94 - 7.03) 0.06 6A/6A - C/C 28 (68.3) 13 (31.7) 3.62 (1.16 - 11.32) 0.03 The p value was determined by Fisher's exact test. OR, odds ratio; 95% CI, 95% confidence interval. Discussion This study surveyed AZD9291 concentration whether the bacterial factor dupA in H. pylori or single nucleotide polymorphisms of MMPs and TIMPs correlated with the susceptibility of gastroduodenal ulcers after H. pylori infection. It shows a rather low prevalence (23.8%) of dupA-positive H.

In addition, the effect of multifactorial intensive therapy on the suppression of nephropathy is selleck chemicals not clear at the advanced stage of overt nephropathy. Bibliography 1. Gaede P, et al. N Engl J Med. 2003;348:383–93. (Level 2)   2. Gaede P, et al. N Engl J Med. 2008;358:580–91. (Level 2)   3. Tu ST, et al. Arch Intern Med. 2010;170:155–61. (Level 4)   Is multifactorial intensive therapy recommended for suppressing the onset of CVD in diabetic nephropathy? Diabetes increases the risk of developing both microvascular complications

and CVD. Many patients who have diabetic nephropathy are complicated with hypertension and dyslipidemia and, therefore, are at an even greater risk of the involvement of CVD. The Steno-2 Study showed the effect of multifactorial intensive 3-deazaneplanocin A datasheet therapy, including blood glucose, blood pressure using RAS inhibitors and lipid control on the progression of nephropathy in type 2 diabetic patients with microalbuminuria. Therefore, multifactorial intensive therapy is recommended for suppressing the involvement of CVD

in early diabetic nephropathy; however, it should be noted that this recommendation is based on a small RCT. In addition, the effect of multifactorial intensive therapy on the suppression of CVD is not clear at the advanced stage of overt nephropathy. Bibliography 1. Gaede P, et al. N Engl J Med. 2003;348:383–93. (Level 2)   2. Gaede, P, et al. N Engl J Med. 2008; 58:580–91. (Level 2)   Chapter 10: IgA nephropathy (IgAN) Clinical EPZ5676 cell line outcomes 1. Clinical course and long-term outcomes   When IgAN was described by Berger and Hinglais in 1968, its prognosis was thought to be favorable. However, after 10- and 20-year outcomes were reported in many countries, including Japan, and ESKD was shown to occur in about 15 and 40 % of cases, the prognosis could no longer be considered favorable. Among

the results from Japan, Asaba et al. reported ESKD in 31 % of patients after 7 years without treatment. Table 5 shows recent Chorioepithelioma reports of renal survival at 10 years in various countries, as summarized by D’Amico. Table 5 Renal survival of IgAN patients in the world Reporter Report year Patient number Average observational period(month) 10-year renal survival (%) Europe  D’Amico G (Italy) 1986 365 79 85  Beukhof et al. (The Netherlands) 1986 75 92 84*  Noel et al. (France) 1987 280 >60 85*  Velo et al. (Spain) 1987 153 >60 81*  Bogenschutz et al. (German) 1990 239 59 81$  Rekola et al. (Sweden) 1990 209 76 83#  Alamartine et al. (France) 1991 282 96 94*  Johnston et al. (UK) 1992 220 65 83#  Payton et al. (UK) 1988 67 – 77*  Manno et al. (Italy)4 2007 437 107 82# Australia  Nicolls et al. 1984 244 60 87#  Ibels et al. 1994 121 107 93* Asia  Woo et al. (Singapore) 1986 151 65 91#  Kusumoto et al. (Japan) 1987 87 114 80*  Katafuchi et al. (Japan) 1994 225 48 74#  Yagame et al. (Japan) 1996 206 110 87#  Koyama et al. (Japan) 1997 448 142 85*  Le et al.

As one can see in this figure, the thermal conductivities of both Si and Ge nanoribbons have a weakly pronounced maximum at low temperatures, T max = 85 K for Si and T max = 91 K for Ge. This property of thermal conductivity temperature dependence is a consequence of rough-edge scattering as the main phonon scattering mechanism at elevated temperatures and the absence of (or weak) anharmonicity

of the lattice potential and correspondingly the absence of (or weak) anharmonic (Umklapp) G418 solubility dmso scattering. The latter causes a clear peak in the thermal conductivity versus temperature both in finite bulk crystals of pure silicon [23] and in low-dimensional nanoribbons [2]. The values of thermal conductivities of the Si and Ge nanoribbons for T > T max

approximately reproduce an isotopic effect because , where v ph is the group velocity of acoustic phonons (see also [22]). The weakly pronounced maximum of the thermal conductivity, at approximately 150 K, was recently observed in Si nanowires in [1]. We want to emphasize in this connection that thermal conductivities of the nanoribbons with the same widths, interparticle potentials, and perfect edges diverge in the limit of N→∞ for all temperatures (see [2]). On the other hand, the buy AICAR obtained suppression of thermal conductivity in the rough-edge nanoribbons for the used value of surface porosity p = Protein Tyrosine Kinase inhibitor 0.20 is not so strong as that for the Si nanowires with rough surfaces which were studied recently in [24] IKBKE (compare Figures 1 and 2 in this work with Figures one and three in [24]). Figure 2 Thermal conductivity κ of rough-edge nanoribbon versus temperature for ribbon length of N = 500 unit cells. Thermal conductivity κ of rough-edge

nanoribbon (ribbon width K = 18 atomic chains, rough edges widths K 1 = 4 atomic chains, porosity of rough edges p = 0.20) versus temperature T for ribbon length of N = 500 unit cells of the two-dimensional diamond-like lattice of Ge (blue circles, line 1) or Si (red diamonds, line 2) atoms. Conclusions Semiquantum molecular dynamics simulations with random Langevin-like forces with a specific power spectral density show that quantum statistics of phonons and porosity of edge layers dramatically change the thermal conductivity of Si and Ge nanoribbons at low and room temperatures in comparison with that of the nanoribbons with perfect edges and classical phonon dynamics and statistics. Phonon scattering by the rough edges and weak anharmonicity of the considered lattice produce weakly pronounced maximum of the thermal conductivity of the nanoribbon at low temperature. The approximate isotopic effect is manifested in the scaling of phonon thermal conductivities of the rough-edge nanoribbons with harmonic lattices at elevated temperature.

Throughout the years of the National Injury Registry, the injury rates in Harstad closely resembled the rates of the national registry [18]. With reference to the recent reports suggesting stabilizing hip fracture incidence internationally as well as nationally, and #BMS-907351 clinical trial randurls[1|1|,|CHEM1|]# regional differences within Norway, we have used the hip fracture data in the Harstad Injury Registry to: 1. Describe age- and sex-specific incidence of hip fractures in Harstad, Northern Norway and make comparison with rates from the Norwegian capital Oslo   2. Describe time trends in hip fracture

incidence in Harstad from 1994 to 2008   3. Describe place of injury and seasonal variations in hip fracture incidence in Harstad   4. Compare 3-month, 6-month, and 1-year mortality after hip fracture between women and men in Harstad   Materials and method The municipality of Harstad, located 250 km north of the Arctic Circle, comprises with its 23,257 inhabitants (January 1, 2010), 0.5% of the Norwegian population. All injured persons, including hip fracture patients, entering the hospital emergency room are recorded in the Harstad Injury Registry. The local hospital, which is the only

hospital in the area, has GF120918 nmr an X-ray department and access to orthopedic surgery, and all patients with hip fractures are treated locally with a minimal leakage to other hospitals. From 1985 to 1993, the registration of hip fractures Fenbendazole was used for evaluation of an injury prevention program [18, 19]. Data from the period between 1985 and 1988 provided baseline information for a 5-year intensive community-based intervention program running between 1989 and 1993, which included removal of environmental hazards in homes, promotion of safe footwear used outdoors and reduction of slippery surfaces in traffic areas during winter. The results indicated a significant reduction of hip fracture rates related to falls indoors and in traffic areas

in winter in men [18]. After 1993, the intervention program continued as an integrated part of the community health service and the present study encompasses the years from 1994 to 2008, after termination of the prevention study. Registration of hip fractures On admission in the hospital, the patient or someone accompanying him/her and the admitting doctor complete an injury registration form providing information concerning name, date of birth, sex, place of residence, activity during injury, time, place and type of injury as well as injury mechanism and body part injured. An open-ended question describes in free text the event leading to the injury. The admitting doctor registers the patient’s diagnosis to the injury registration form, usually based on the present clinical symptoms. The forms are collected and examined by a specially trained nurse who also assures that all incidents are registered by comparing with the admission list. She then enters the data into a common database.

Infect Immun 2005, 73:7161–7169.CrossRefPubMed 25. Methner U, Barrow PA, Gregorova D, Rychlik I: Intestinal colonisation-inhibition and virulence of Salmonella phoP, rpoS and ompC deletion mutants in chickens. Vet Microbiol 2004, 98:37–43.CrossRefPubMed 26. Datsenko KA, Wanner BL: One-step inactivation of chromosomal genes in Escherichia coli K-12 using PCR products. Proc Natl Acad Sci USA 2000, 97:6640–6645.CrossRefPubMed Authors’ contributions

DK and AS constructed the SPI mutants, FS, HH, AMS and AI were responsible for the animal experiments. see more VK and BN analysed the samples by histology scoring and JV performed the cytokine expression by RT PCR. IR together with BN designed the experiments and wrote the manuscript. All authors read and approved the final manuscript.”
“Background The Roseobacter clade is a lineage of

the Rhodobacteraceae within the Alphaproteobacteria. It is the most abundant and diverse group of marine Gram-negative, non-obligately phototrophic prokaryotes. They represent up to 25% of marine communities, especially in coastal and polar regions [reviewed in [1, 2]]. Currently, 41 subclusters are described, covering all major oceanic habitats like seawater, algal blooms, microbial mats, sediments, sea ice and marine invertebrates [2]. Members of the Roseobacter clade display Selleckchem Baf-A1 diverse www.selleckchem.com/products/VX-680(MK-0457).html physiologies. For example, some members can generate energy via aerobic anoxygenic photosynthesis, oxidize the green-house gas carbon monoxide and produce the climate-relevant gas dimethylsulfide through the degradation of different sulphur compounds. Thereby, these bacteria significantly influence the global carbon and sulphur cycles as well as the climate [2]. Moreover, they are able to degrade aromatic

compounds, reduce trace metals, produce bioactive secondary metabolites, perform quorum sensing and can establish symbiotic and pathogenic relationships [1–5]. Several members of the Roseobacter clade have been implicated as causative agents of juvenile oyster disease in Eastern Dichloromethane dehalogenase oyster and black band disease in scleractina coral [2, 6], or were described as probiotics for fish larvae [7, 8]. Scientific interest in this bacterial group increased steadily since the description of its first representatives Roseobacter denitrificans and Roseobacter litoralis [9]. Since the first genomes of Silicibacter pomeroyi and R. denitrificans have been completely elucidated [10, 11] a massive genome sequencing approach financed by the Gordon & Betty Moore foundation resulted in currently 23 draft and 5 finished genome sequences from the Roseobacter clade.

putida [9, 13]. Thus, BenR-CatR

or BenM-CatM regulation may serve as a practical model for complex regulatory circuits involved in the biodegradation of benzoate. Aromatic compounds are not preferred as growth substrates. In most cases, synthesis of the catabolic enzymes is reduced when certain rapidly metabolizable carbon sources are simultaneously present [14]. One such control mechanism is called catabolite repression, which can integrate different signals, thus increasing the Selleckchem Trichostatin A complexity of the system [15]. Although the molecular mechanism responsible for global control is not yet well understood, available data suggest that catabolite repression control (Crc) is a component of a signal transduction pathway that modulates carbon metabolism in some soil bacteria. In addition, Crc has also been observed in several Pseudomonas species [16]. Very recently, A. baylyi Crc was proposed to be involved click here in determining the transcript stability of the pca-qui operon, thereby mediating catabolite repression [17]. The β-ketoadipate pathway is found almost exclusively in soil microorganisms, especially in Pseudomonas species, emphasizing the importance of aromatic compound catabolism in this family [18, 19]. Establishment of the complete genome sequence of Pseudomonas strains enabled mapping of the entire catabolic gene cluster in their chromosomes [2, 20,

21]. Despite the current extensive knowledge about the aerobic catabolism of aromatic compounds in Pseudomonas strains, there remains much more to understand. For Interleukin-2 receptor instance, the large information

gap between sequence information and function for genes responsible for aromatic catabolism is a major challenge to the field of functional genomics. In particular, the evolutionary and regulatory mechanisms of aromatic catabolic pathways in the nitrogen-fixing and root-associated bacteria have been poorly documented. P. stutzeri A1501 was isolated from paddy soil in South China in the early 1980s for its ability to fix nitrogen under microaerobic conditions in the free-living state and to colonize rice endophytically [22–24]. As previously mentioned, aromatic compounds are highly abundant in the soil, so they can serve as a normal carbon source for A1501 when this bacterium colonizes on root surfaces of host plants. In this study, genomic analysis showed that A1501 contains sets of genes encoding enzymes and regulators involved in the biodegradation of benzoate and 4-hydroxybenzoate. Herein, we present evidence that benzoate degradation is subject to catabolite repression control. We also describe, for the first time, that low concentrations of 4-hydroxybenzoate Selleck GDC-941 significantly enhance the ability of A1501 to degrade benzoate. Results Genome-wide analysis of the aromatic catabolism pathways P.

Low levels of #GDC-0068 chemical structure randurls[1|1|,|CHEM1|]# this endogenous antioxidant in the cocoa supplemented animals may be due to the higher bioavailability of exogenous antioxidants derived from the cocoa. The accumulation of exogenous antioxidants from cocoa may therefore be beneficial in providing sufficient antioxidants to quench ROS in NASH. Our findings on hepatic GSH are not in agreement with most other studies which show a depletion of this endogenous antioxidant [7]. Despite the novel data presented from the current study there are limitations associated with the findings. Due to restrictions imposed by the institutional animal welfare committee it

was not possible to include additional MCD fed rats for 80 and 108 days to match cocoa supplementation groups C1 – C4.

Although pilot data indicated histologically the livers of rats fed the MCD diet are similar from 42 CP673451 purchase – 112 days, it cannot be excluded that the effects associated with cocoa supplementation in the liver are not to prolonged MCD feeding. It is possible, but unlikely, that the results observed following cocoa supplementation are not due to the antioxidants present in the cocoa, but rather the trace amounts of methionine and choline present in the cocoa. However if the trace amounts of methionine and choline present in the cocoa were responsible for the results observed it would be expected that data collected from the cocoa supplemented groups would more closely resemble the MCS group and not the MCD group. Finally although the MCD diet is a commonly used model of NASH there are a number of limitations associated with comparing the model to metabolic changes in human NAFLD/NASH [7]. These limitations include weight loss in rats fed the MCD diet, whereas NASH patients are typically overweight or obese [1, 7]. The accumulation

of fat within the liver of rats fed the MCD diet is due to a disruption of the export of hepatic lipids and subsequent lipotoxicity, unlike the human situation where the excessive hepatic fat import or storage is thought to occur [1, 7]. Conclusions Our investigations indicate that the intracellular lipid transporter LFABP may play a key role in the establishment of MCD induced NAFLD and NASH not only by shuttling long chain fatty acids within the cell, but possibly by also acting as an antioxidant. Furthermore, Staurosporine in vivo the decreased levels of LFABP in the MCD model of NASH may suggest impairment in the functioning of LFABP in this disease. A cocoa rich diet is able to act as a rich source of exogenous antioxidants with no depletion of RBC GSH. However, this does not lead to lower hepatic superoxide and 8-OH-2dG levels. During the supplementation with the C1 diet regime, cocoa was associated with higher levels of LFABP compared to the MCD diet. There is depletion in the levels of NOX1 mRNA in animals on the MCD diet. NOX1 however is higher at the protein level in the animals on the C2 regime.

Table 1 Primers Primer Sequence Reference 27 F 5′AGAGTTTGATCMTGGCTCAG-3′ [13] 341 5′-CCTAYGGGRBGCASCAG-3′ [14, 15] 806 5′-GGACTACNNGGGTATCTAAT-3′ [14, 15] TitA_341F 5′-CGTATCGCCTCCCTCGCGCCATCAG-TAG-CCTAYGGGRBGCASCAG-3′ [16] TitB_806R 5′-CTATGCGCCTTGCCAGCCCGCTCAG-GGACTACNNGGGTATCTAAT-3′ [16] 1492R 5′-GGTTACCTTGTTACGACTT-3′

[13] In the second PCR the adaptors were attached to the amplicon library elongating the fragment towards 526 bp with the primer TitA_341F and TitB_806R. The same reaction conditions of PCR I were applied in PCR II with a reduced cycle number of 15. Initially we tried to apply the same ACY-738 clinical trial procedure for the lung tissue samples but unspecific bands after gel-electrophoresis made it impossible to select the correct fragment size. To overcome this problem we chose the primer 27 F and 1492R amplifying MK-8931 datasheet the entire 16S rRNA gene which appeared to be more specific. The PCR I conditions were the same as mentioned above except that the annealing temperature was reduced to 55°C and the cycle number to 40. In this perspective the Tag-PCR reaction with TitA_341F and TitB_806R provided the selection for V3 and V4 as well as attaching the adaptors to the amplicons. Statistical analysis and bioinformatics The 16S rRNA gene sequences obtained from one half a plate of a 454 – Roche

– Titanium pyrosequencing run were quality filtered, trimmed and split into the corresponding animal samples with the Qiime pipeline version 1.6.0 using the default settings [17]. We considered only sequences with a minimum

length of 250 bp. Chimeras were removed by UCHIME [18]. The operational taxonomic units (OTU) were picked de novo and clustered at 97% sequence similarity. selleck kinase inhibitor The taxonomy was assigned using RDP classifier (bootstrap threshold 0.8) greengenes as reference database [19]. For statistical analysis, raw data were transferred into the open source statistical program “R” [20]. The non-parametric Wilcoxon test (W) evaluated variations of alpha diversity between two variables. We used the non-parametric Kruskal-Wallis-test when APR-246 price comparing more than 2 variables (KW). Dissimilarities in OTUs abundance between the samples were explained by KW and the sample clustering of the OTU count based Bray-Curtis distance metric were examined by the analysis of similarity (anosim). Results To determine the airway bacterial microbiota of the BALB/cJ mouse model based on 16S rDNA gene sequencing, we have compared sequences found in the lungs with three different approaches, to sequences found in corresponding vaginal and caecal samples. Over all sequence quality and results from all sample types We generated a total of 908256 sequences. After quality filtering and chimera check, 27% of sequences were removed and 660319 sequences were further processed for OTU picking (sequences ranged between 3530 up to 31638 per animal sample).

g., selleck chemicals Hoffmann 1998). He was—in the best sense—a traditional educated scholar with high ethical standards and had a deep feeling for the responsibility of scientists to protect and preserve life on earth. Paul Hoffmann is survived by his wife and two daughters. We will remember him as a highly esteemed teacher and supervisor, organizer, prolific researcher and a dear colleague. AZD5363 purchase The “Sonderforschungsbereich”

429 will hold a commemorative colloquium to honor Professor Dr. Paul Hoffmann in 2009. We end this tribute by showing three pictures of Paul Hoffmann interacting with several colleagues. Figures 3 and 4 are pictures taken at the “German-Belarus Symposium on Biophysics of Photosynthesis”, Egsdorf, Germany, 2003—probably the last international meeting that Hoffmann attended. Figure 5 shows a photograph of Hoffmann together with other scientists after Govindjee delivered a lecture at the Humboldt University in 2006. Fig. 3 Professor Paul Hoffmann (third

from left) among the participants of the “German-Belarus Symposium on Biophysics of Photosynthesis,” Egsdorf, Germany, 2003. Other participants included: Vladimir Shuvalov, Olga Kaminskaya, Vyacheslav Klimov, Elena Yaronskaya, Wolfhard Rüdiger, Nikolai MI-503 Shalygo, Natalia Averina, Igor Volotovski, Hugo Scheer, Bernhard Grimm, Peter Jahns, Ljudmilla Kalituho, Carsten Tietz, Gernot Renger, Harald Paulsen, Heiko Lokstein, and Dieter Leupold Fig. 4 Professor Paul Hoffmann (left) together with Igor Volotovsky (middle) and Gernot Renger (right), at the “German-Belarus Symposium on Biophysics of Photosynthesis,” Egsdorf, Germany, 2003 Fig. 5 Professor Paul Hoffmann (3rd from right) together with Günter Döring, Ulrich Siggel, Gernot Renger, Govindjee and Annegret Wilde (from left to right) at Humboldt Histamine H2 receptor University Berlin, Germany, 2006. Courtesy of Govindjee Acknowledgment We thank Govindjee for editing this manuscript. References Govindjee, Šesták Z, Peters WR (2002) The early history of “Photosynthetica”, “Photosynthesis research”, and their publishers. Photosynthetica 40:1–11. doi:10.​1023/​A:​1020169502548

CrossRef Hoffmann P (1962a) Untersuchungen über Photosynthese und Atmung von Laubblättern verschiedenen Alters. Flora 152:622–654 (in German) Hoffmann P (1962b) Der Einfluß von Wirkstoffen auf die Photosynthese und Atmung alternder Laubblätter. Flora 152:702–706 (in German) Hoffmann P (1968) Zur Physiologie der Photosynthese bei höheren Pflanzen. Botanische Studien, Jena. 18:151 (in German) Hoffmann P (1975) Photosynthese (in German). WTB 158, Akademie-Verlag, Berlin Hoffmann P (1987) Fotoszintézis (translated to Hungarian by Z. Szigeti). Mezőgazdasági Kiadó, Budapest, p 249 Hoffmann P (1998) Oxygenic photosynthesis—a photon driven hydrogen generator—the energetic/entropic basis of life. Photosynthetica 35:1–11. doi:10.