Limited studies on the relationship between tablet shape, selleck chemical size and the splitter model and the accuracy of splitting. In this

work, divisibility of tablets with various shapes and sizes for medicines normally split was studied using a kitchen knife and four tablet splitter models. Results demonstrated deviation in tablet fragments weight changes with tablet shape, size and splitter model. The tablets-related factors (shape and size) and the splitter model are critical parameters in splitting of tablets. Splitting of tablets into halves and quarters to obtain a suitable unit dose is frequently done using a variety of methods.1 A significant deviation in weight from the theoretical value for tablet halves and quarters on splitting using scissors, hands and one tablet splitter model.2 In this work, a kitchen knife and four tablet splitter models were tested for splitting of tablets having different shapes and sizes for medicines normally split. Tablets from furosemide 40 mg (circular shape, unscored), captopril 50 mg (square shape, bisected both sides), spirolactone 100 mg (circular shape, scored), enalpril 10 mg (heart shape,

scored) and paracetamol 500 mg (caplet, scored) were first assessed for diameter/length, thickness and hardness. From each medicine, ten randomly selected tables were individually weight using a sensitive balance, split into halves and into quarters using a kitchen knife and splitter learn more models; Pillmate (P), Fortuna (F), Safe Sound (S) and Health Care (H). The weight variation for 10 intact tablets, 20 halves and 40 quarters for each medicine was calculated using United States Pharmacopoeia (USP) criteria for intact tablets. Weight loss was determined by subtracting the weight of the two tablet halves

or four quarters from the weight of intact Buspirone HCl tablet. Statistical analysis of data was performed using t-test at P value less than 0.05 as significant. The average diameter/length, thickness and hardness of tablets were (8, 10, 9.6, 8 and 17.7 mm), (2, 4, 4, 4 and 5 mm) and (7, 11, 9, 10 and 8 Kp) for furosemide, captopril, spirolactone, enalpril and paracetamol. The relative standard deviation (RSD) values of weight were between 1.0–1.6, 8.4–15.2 and 17. 2–26.7% for intact tablets, halves and quarters respectively after splitting using a kitchen knife and tablet splitter models (P, F, S and H). Tablet fragments deviated in weight by more than 15% from the theoretical values were 10, 20, 37, 22 and 4% for halves and 35, 48, 53, 58 and 35% for quarters. The associated tablet weight loss ranges were 0.5–1, 1–7, 0–5, 0–3 and 0–2% after halving and 2–3, 2–9, 1–12, 1–5 and 1–4% after splitting into quarters.

Zidovudine treatment increased the expression of cytokeratin 10, PCNA and cyclin A. Conversely, cytokeratin 5, involucrin and cytokeratin 6 expression was decreased. The tissue exhibited characteristics of increased proliferation in the suprabasal

layers as well as an increased fragility and an inability to heal itself. Zidovudine treatment, even when applied at low concentrations for short periods of time, deregulated the cell cycle/proliferation and differentiation pathways, resulting in abnormal epithelial repair and proliferation. Our system could potentially be developed as a model for studying the effects of HIV and highly active antiretroviral therapy in vitro. An estimated 33.4 million people are infected with HIV world-wide [1]. The advent of antiviral drugs has greatly decreased mortality from this virus Selumetinib manufacturer and improved the life expectancy of HIV-infected patients. Highly high throughput screening compounds active antiretroviral therapy

(HAART), which consists of therapy with a combination of reverse transcriptase inhibitors and protease inhibitors, is able to greatly reduce the HIV viral load of patients and help to restore their immune function. However, continuous drug regimens and the patients’ ability to live longer with a suppressed immune system have led to complications. Oral complications are very common in HIV-positive patients. The incidence of the oral complications oral candidiasis and oral hairy leukoplakia has been shown to drop significantly in patients on ID-8 HAART [2-4]. Other oral complications that are common in HIV-positive patients, such as Kaposi’s sarcoma and oral aphthous ulceration, have been shown to be unaffected by HAART [2, 3, 5]. Long-term use of

HAART has been associated with increases in the rates of many complications, including oral warts [2, 5], erythema multiforme [6, 7], xerostomia [6, 7], toxic epidermal necrolysis, lichenoid reactions [7, 8], exfoliative cheilitis [6], oral ulceration and paraesthesia [6, 9]. Such adverse oral complications greatly affect the quality of life of patients on HAART, leading to noncompliance with drug regimens. This in turn results in interrupted dosing schedules and suboptimal levels of exposure to the drugs. Nonadherence to a strict drug regimen could eventually lead to drug resistance and compromise future therapy [10]. Nucleoside reverse transcriptase inhibitors (NRTIs), such as zidovudine [ZDV; formerly azidothymidine (AZT) or 3'-azido-3'-deoxythymidine], were first approved by the US Food and Drug Administration for use against HIV/AIDS in 1987 [11]. ZDV has become an essential component of HAART and has a two-pronged antiviral effect. It disrupts the virus both by incorporating itself into viral DNA and by inhibiting the viral reverse transcriptase [11]. ZDV also exhibits some affinity for cellular polymerases [12, 13].

vaginalis, the aim of this study was to characterize ADA activity, an enzyme involved in nucleoside metabolism, and to evaluate the relative mRNA expression of ADA-related genes in this

mucosal parasite. Trichomonas vaginalis clinical isolate TV-VP60 (Michel et al., 2006) was used throughout this enzyme characterization study. The other five isolates were TV-30236 (from the American Type Culture Collection, ATCC) and the clinical isolates TV-LACM1, TV-LACM2, TV-LACH1 and TV-LACH2 from our Clinical Laboratory surveys (Universidade Federal do Rio Grande do Sul, Brazil). Trichomonads were cultured axenically in vitro and maintained in trypticase–yeast extract–maltose (TYM) medium (Diamond, 1957), pH 6.0, supplemented with 10% (v/v) inactivated bovine serum at 37 °C. Organisms from the logarithmic phase were evaluated before and after assays based on motility and viability using trypan blue (0.2%) exclusion. The parasites were then harvested by centrifugation PI3K inhibitor and washed three times with phosphate-buffered saline (PBS) added with 2.0 mM EDTA and 2.0 mM EGTA. The final pellet was resuspended and used for the subsequent assays.

Trichomonas vaginalis lysates were obtained in liquid nitrogen, at 0.1 mg−1 protein−1 mL−1, in the presence of 1.0 mM protease inhibitor cocktail. An aliquot from the parasite suspension was added to the reaction mixture containing 50 mM sodium phosphate buffer (pH 7.5) to maintain the protein concentration (50–150 μg mL−1) in the final volume of 200 μL. The samples were then preincubated for 10 min at 37 °C. The selleck screening library reaction was initiated with the addition of the substrate adenosine (3.0 mM) and stopped, after a determined time (10–40 min), by adding the samples on 500 μL of phenol-nitroprusside reagent (50.4 mg of phenol and 0.4 mg of sodium nitroprusside mL−1). Controls with the addition of the enzyme preparation after the termination of reaction were used to correct nonenzymatic deamination of the substrate. The reaction mixtures were mixed with 500 μL of alkaline-hypochlorite reagent (sodium hypochlorite to 0.125% available chlorine, in 0.6 M PtdIns(3,4)P2 NaOH). Samples were incubated at 37 °C for 15 min. The colorimetric

assay was carried out at 635 nm (Giusti, 1974) to measure the ammonia produced by the enzymatic reaction and the ADA activity was expressed as nmol NH3 min−1 mg−1 protein. In all assays, at least three different experiments were performed in triplicate. The protein quantification was performed in triplicate for the parasite suspensions (Bradford, 1976) using bovine serum albumin as a standard. After the standardization of incubation time and the protein concentration in order to maintain the linearity of the enzymatic reaction, assays to determine the optimum pH were performed using 50 mM sodium phosphate buffer (mixture: 0.2 M disodium phosphate and 0.2 M sodium phosphate, pH 6.5–7.5) and sodium carbonate bicarbonate buffer (mixture: 0.2 M sodium carbonate and 0.

4%) had a significant (fourfold or greater) increase in titre after vaccination (Table 2). In contrast, only eight patients (6.3%) had an antibody titre ≤ 1:10. These differences were found to be statistically significant (χ2 = 61.09; P < 0.0001). No correlation was found between age Idasanutlin molecular weight and pre-vaccination HI titre. In the χ2 analysis, a nonsignificant trend for a higher proportion of patients with HI titres ≥ 1:40 (P = 0.083) in the > 60 years old group was found; 13 of 19 patients (68.4%) in the > 60 years old group had HI titres

≥ 1:40 compared with 88 of 199 patients (48.9%) in the ≤ 60 years old group. The SPR, SCR and mean increase in GMT in the ≤ 60 years old group were 91.2%, 68.1% and 2.43 ± 0.51, respectively. In the > 60 years old group, the SPR, SCR and mean increase in GMT were 92.3%, 61.5% and 2.32 ± 0.52, respectively. In the univariate analysis, ART status, VL and baseline H1N1 antibody titres were found to be significantly associated with H1N1 antibody titres of ≥ 1:40. Nine of 16 patients (56%) not on treatment did not achieve antibody titres required for seroprotectivity. In contrast, 79 of 110 patients

(72%) on treatment achieved HI antibody levels ≥ 1:40. Lower Selleck BIBW2992 HIV VL and higher baseline HI H1N1 antibody titres were also associated with higher post-vaccination HI titres. Further analysis found that only 12 of 26 patients (46%) with detectable VL, but 74 of 100 patients (74%) with undetectable VL (< 50 copies/mL), achieved antibody titres ≥ 1:40 (χ2 = 7.384; P = 0.007). VL and baseline HI H1N1 antibody titre were found to be the predictors of

a response to vaccination (≥ 1:40) in the BLR model (χ2 = 15.71; d.f. = 2; P < 0.0001) (Table 3). The model correctly predicted 71.4% of cases. The Hosmer–Lemeshow goodness of Thalidomide fit statistic showed that the model was good (P > 0.05). During the Southern Hemisphere winter of 2009 there was considerable concern about the impact of the H1N1 influenza virus as it started spreading within the general population, particularly in those considered at increased risk for complications. Clinics dealing with high-risk patients were disseminated free vaccines via the State’s Public Health Units for mass immunization. HIV-infected patients were considered to be at greater risk of complications from H1N1 infection compared with the general population, although subsequent audits from a number of large HIV centres have suggested that the opposite was actually true. Patients with HIV-1 infection have been shown to have weaker responses to seasonal influenza vaccination, with lower antibody response rates being associated with lower CD4 T-cell count, not being on ART and previous AIDS, with an impaired response being anticipated to H1N1 09 vaccination in this population [8].

Multivariate logistic regression analyses were conducted to assess characteristics associated with never having

been tested for HIV. Of the 13 111 participants, 26% were untested. By size of population, untested MSM were more likely to live in cities with fewer than 500 000 inhabitants (60% versus 44% for tested MSM; P < 0.05). In general, untested MSM were more likely to be younger than 25 years old (43% versus 16% for tested MSM; P < 0.05), with a median age of 26 years versus 33 years for tested MSM. Using the International Standard Classification of Educational Degrees to categorize education level, most untested MSM had a medium (38% versus 30% for tested MSM; P < 0.05) or low (11% versus 8% for tested MSM; P < 0.05) level of education. Regarding employment, untested MSM were significantly

JQ1 chemical structure more likely to be students selleck compound (32% versus 12% for tested MSM; P < 0.05) compared with tested MSM. More untested MSM identified themselves as bisexual (18% versus 10% for tested MSM; P < 0.05) or had not yet defined their sexual identity (10% versus 7% for tested MSM; P < 0.05). In comparison with tested MSM, fewer untested MSM had visited commercial gay venues (72% versus 90% for tested MSM; P < 0.05) and sex venues (47% versus 68% for tested MSM; P < 0.05) in the last 12 months. The number of nonsteady partners was lower among untested than among tested MSM. Men who reported fewer than three partners or no nonsteady partner in the last 12 months were more likely to be untested (54% versus 32% for tested MSM; P < 0.05). Unprotected anal intercourse (UAI) with a steady partner was more frequent among untested MSM (76% versus 73% for tested MSM; P < 0.05). There was Docetaxel in vivo no significant difference between the untested and tested MSM in relation to UAI with nonsteady partners in the last 12 months (45% versus 47%, respectively; P > 0.05). A higher proportion of untested MSM had UAI

with a steady partner whose HIV status was unknown or discordant (30% versus 7% for tested MSM; P < 0.05). The nonuse of drugs in the last 12 months was more common among untested MSM than among tested MSM (64% versus 43%, respectively; P < 0.05). Almost five times fewer untested MSM than tested MSM had had a diagnosis of an STI (syphilis, gonorrhea, chlamydia, genital warts or herpes) in the last 12 months (3% versus 14%, respectively; P < 0.05). Overall, more untested MSM perceived that they did not have access to free or affordable HIV testing (31% versus 7% for tested MSM; P < 0.05) and felt less confident to access HIV testing than tested MSM (13% versus 3%, respectively; P < 0.05). Multivariate analysis confirmed some factors as being associated with never having been tested among MSM (Table 1): being younger than 25 years old [odds ratio (OR) 2.9; 95% confidence interval (CI) 2.5–3.4], living in settlements with fewer than 500 000 inhabitants (from OR 1.

5). Following early somatosensory

attention effects, both endogenous tasks showed modulations at N140 and Nd with larger negativity for expected compared with unexpected trials. For topographical maps of the effects, see Fig. 6. No significant main effects or interactions involving the factor Cue were found for the P45 analysis window. Analysis of the N80 time window showed a Task × Cue × Hemisphere interaction (F2,22 = 21.39, P < 0.001,  = 0.66), as well as a Cue × Hemisphere interaction (F1,11 = 7.40, P = 0.02,  = 0.40). This interaction was broken down further and each task was analysed separately. The exogenous task showed a significant Cue × Hemisphere effect (F1,11 = 29.51, P < 0.001,  = 0.73), and separate

follow-up analyses for each hemisphere showed a significant effect of Cue (F1,11 = 10.01, P = 0.009, check details PD0325901 manufacturer  = 0.48) over electrodes contralateral to the target location, whilst no attention effect was seen over ipsilateral electrodes. There was no correlation between contralateral attention modulation and RT effect (r = 0.04, n.s.). In other words, there was no indication that larger attention modulation of the N80 related to a larger RT effect across participants. In the endogenous predictive task there was a Cue × Hemisphere interaction (F1,11 = 12.00, P = 0.005,  = 0.52), and separate follow-up analyses for each hemisphere showed Carteolol HCl an attention effect over electrodes contralateral to target presentation only (Cue: F1,11 = 5.19, P = 0.044,  = 0.32). There was no significant correlation between the contralateral attention modulation and RT effect (r = 0.52, n.s.). The endogenous counter-predictive task also demonstrated a significant Cue × Hemisphere interaction (F1,11 = 12.97, P = 0.004,  = 0.54), and separate follow-up analyses of each hemisphere demonstrated the N80 attention effect to be present only at electrodes ipsilateral (Cue: F1,11 = 6.97, P = 0.023,  = 0.39) to target location. There was no significant correlation between

ipsilateral attention modulation and RT effect (r = 0.32, n.s.). The overall analysis including all three tasks at the P100 time window demonstrated a significant Task × Cue × Hemisphere interaction (F2,22 = 8.47, P = 0.002,  = 0.44), as well as a Cue × Hemisphere interaction (F1,11 = 15.95, P = 0.002,  = 0.59), and follow-up analyses were conducted for each task separately. The exogenous task showed a significant Cue × Hemisphere interaction (F1,11 = 12.25, P = 0.005,  = 0.53). However, separate follow-up analysis revealed no significant effect of attention at either hemisphere. In the endogenous predictive task there was a Cue × Hemisphere interaction (F1,11 = 14.54, P = 0.003,  = 0.57), and separate follow-up analyses for each hemisphere showed a Cue × Electrode site interaction at contralateral electrodes (F5,55 = 7.07, P = 0.001,  = 0.39).

Furthermore, human imaging studies that have tried to delineate cortical areas modulating their blood oxygenation level-dependent (BOLD) response with set size have yielded contradictory results. In order to test whether BOLD imaging of the rhesus monkey cortex yields results consistent with the electrophysiological findings and, moreover, to clarify if additional other cortical regions

beyond the two hitherto implicated are involved in this process, we studied monkeys while performing a covert visual search task. When varying the number of distractors in the search task, we observed a monotonic increase in error rates when search time was kept constant as was expected if monkeys

resorted to a serial search strategy. Visual search consistently evoked robust BOLD activity in the Metabolism inhibitor monkey FEF and PD0325901 order a region in the intraparietal sulcus in its lateral and middle part, probably involving area LIP. Whereas the BOLD response in the FEF did not depend on set size, the LIP signal increased in parallel with set size. These results demonstrate the virtue of BOLD imaging in monkeys when trying to delineate cortical areas underlying a cognitive process like visual search. However, they also demonstrate the caution needed when inferring neural activity from BOLD activity. “
“Department of Neuroscience, University Medical Centre (CMU), Geneva, Switzerland Ernst Strüngmann Institute (ESI) for Neuroscience in Cooperation with Max Planck Society, GNA12 Frankfurt, Germany We investigated the effect of eye-in-head and head-on-trunk direction on heading discrimination. Participants were

passively translated in darkness along linear trajectories in the horizontal plane deviating 2° or 5° to the right or left of straight-ahead as defined by the subject’s trunk. Participants had to report whether the experienced translation was to the right or left of the trunk straight-ahead. In a first set of experiments, the head was centered on the trunk and fixation lights directed the eyes 16° either left or right. Although eye position was not correlated with the direction of translation, rightward reports were more frequent when looking right than when looking left, a shift of the point of subjective equivalence in the direction opposite to eye direction (two of the 38 participants showed the opposite effect). In a second experiment, subjects had to judge the same trunk-referenced trajectories with head-on-trunk deviated 16° left. Comparison with the performance in the head-centered paradigms showed an effect of the head in the same direction as the effect of eye eccentricity. These results can be qualitatively described by biases reflecting statistical regularities present in human behaviors such as the alignment of gaze and path.

Furthermore, human imaging studies that have tried to delineate cortical areas modulating their blood oxygenation level-dependent (BOLD) response with set size have yielded contradictory results. In order to test whether BOLD imaging of the rhesus monkey cortex yields results consistent with the electrophysiological findings and, moreover, to clarify if additional other cortical regions

beyond the two hitherto implicated are involved in this process, we studied monkeys while performing a covert visual search task. When varying the number of distractors in the search task, we observed a monotonic increase in error rates when search time was kept constant as was expected if monkeys

resorted to a serial search strategy. Visual search consistently evoked robust BOLD activity in the Y-27632 supplier monkey FEF and selleck products a region in the intraparietal sulcus in its lateral and middle part, probably involving area LIP. Whereas the BOLD response in the FEF did not depend on set size, the LIP signal increased in parallel with set size. These results demonstrate the virtue of BOLD imaging in monkeys when trying to delineate cortical areas underlying a cognitive process like visual search. However, they also demonstrate the caution needed when inferring neural activity from BOLD activity. “
“Department of Neuroscience, University Medical Centre (CMU), Geneva, Switzerland Ernst Strüngmann Institute (ESI) for Neuroscience in Cooperation with Max Planck Society, ever Frankfurt, Germany We investigated the effect of eye-in-head and head-on-trunk direction on heading discrimination. Participants were

passively translated in darkness along linear trajectories in the horizontal plane deviating 2° or 5° to the right or left of straight-ahead as defined by the subject’s trunk. Participants had to report whether the experienced translation was to the right or left of the trunk straight-ahead. In a first set of experiments, the head was centered on the trunk and fixation lights directed the eyes 16° either left or right. Although eye position was not correlated with the direction of translation, rightward reports were more frequent when looking right than when looking left, a shift of the point of subjective equivalence in the direction opposite to eye direction (two of the 38 participants showed the opposite effect). In a second experiment, subjects had to judge the same trunk-referenced trajectories with head-on-trunk deviated 16° left. Comparison with the performance in the head-centered paradigms showed an effect of the head in the same direction as the effect of eye eccentricity. These results can be qualitatively described by biases reflecting statistical regularities present in human behaviors such as the alignment of gaze and path.

For this study, C57BL/6N male mice were subjected to a 60-min middle cerebral artery occlusion, and were given 50 mg/kg/day metformin beginning 24 h post-stroke for 3 weeks. Behavioral recovery was assessed using adhesive-tape removal and the apomorphine-induced turning test. The role of angiogenesis was assessed by counting vessel branch points SAR245409 from fluorescein-conjugated lectin-perfused brain sections. Importantly even if metformin treatment was initiated 24 h after injury it enhanced recovery and significantly improved stroke-induced behavioral deficits. This

recovery occurred in parallel with enhanced angiogenesis and with restoration of endogenous cerebral dopaminergic tone and revascularization of ischemic tissue. We assessed if the effects on recovery and angiogenesis were mediated by AMPK. When tested in AMPK α-2 knockout mice, we found that metformin treatment did not have the same beneficial effects on recovery and angiogenesis, suggesting that metformin-induced angiogenic effects are mediated by AMPK. The results from this study suggest that metformin mediates post-stroke recovery by enhancing angiogenesis, and these effects are mediated by AMPK signaling. “
“Mammalian Dabrafenib research buy retina harbours a self-sustained

circadian clock able to synchronize to the light : dark (LD) cycle and to drive cyclic outputs such as night-time melatonin synthesis. Clock genes are expressed in distinct parts of the tissue, and it is presently assumed that the retina contains several circadian oscillators. However, molecular organization of cell type-specific clockworks has been

poorly investigated. Here, we questioned the presence of a circadian clock in rat photoreceptors by studying 24-h kinetics of clock and clock output gene expression in whole photoreceptor layers isolated by vibratome sectioning. To address the importance of light stimulation towards photoreceptor clock properties, animals were exposed to 12 : 12 h LD cycle or 36 h constant darkness. Clock, Bmal1, Per1, SSR128129E Per2, Cry1, Cry2, RevErbα and Rorβ clock genes were all found to be expressed in photoreceptors and to display rhythmic transcription in LD cycle. Clock genes in whole retinas, used as a reference, also showed rhythmic expression with marked similarity to the profiles in pure photoreceptors. In contrast, clock gene oscillations were no longer detectable in photoreceptor layers after 36 h darkness, with the exception of Cry2 and Rorβ. Importantly, transcripts from two well-characterized clock output genes, Aanat (arylalkylamine N-acetyltransferase) and c-fos, retained sustained rhythmicity. We conclude that rat photoreceptors contain the core machinery of a circadian oscillator likely to be operative and to drive rhythmic outputs under exposure to a 24-h LD cycle. Constant darkness dramatically alters the photoreceptor clockwork and circadian functions might then rely on inputs from extra-photoreceptor oscillators.

In the heterogeneous populations studied here, the cumulative incidence of LTBI averaged 2.0% (99% CI: 1.6–2.4), as measured by the TST, with a range in individual study estimates from 0.96% to 3.59%. This result was likely influenced by false positives due to the limitations of the TST and the likelihood Small molecule library order of false positive test results in a low-prevalence population. To maximize PPV of either the TST or an IGRA, we suggest

an individualized risk-based approach, targeting higher-risk, long-term military and civilian travelers based on their duration of travel, the TB endemicity of the country to which they travel, the type of activities in which they will engage, and how closely they will interact with the local population, particularly in an indoor setting. Such

targeted testing has already been recommended by the CDC,13 the Canadian Public Health Agency,16 and the US Air Force.23 Additional studies are needed among international traveler populations to identify more precise population- and individual-level factors that are associated with both differential risk for LTBI and risk of progression to active disease, and that can be both generalized and applied on a regional basis. This type of knowledge would assist in the development of better targeted testing recommendations. Data sources should include travel clinics that service civilian and governmental check details populations, militaries that deploy outside their home country, and multinational corporations that may have large numbers of expatriates living in nations with a high TB prevalence. Heterogeneous populations should be studied to further explore causes of heterogeneity in risk for LTBI, such as lengths of travel, activities performed, and location of travel. Since the heterogeneity inherent in the population of long-term travelers may be a source of unmeasured confounding, a careful intra- or post-travel exposure assessment and attention to demonstrated risk factors is critical in obtaining an unconfounded Oxalosuccinic acid estimate of risk. Individual risk factors should be accounted for, such as being foreign-born, visiting friends and relatives, engaging

in health care activities, having HIV infection or other immunosuppressive comorbidities, as these populations may be at greatest risk for exposure to or infection with TB. Additional variables that should be measured include infection with NTM and history of BCG vaccination. Prospective testing using two-step TST with comparison IGRA, and including intra-travel and post-travel testing with follow-up to active TB would contribute valuable data but may be resource-intensive and cost-prohibitive. We would like to thank the following persons for their data and review contributions: Dr Ingo Fengler, Oberstabsarzt, Facharzt für Mikrobiologie und Infektionsepidemiologie, ZInstSanBW Koblenz, LabAbt I, Mikrobiologie; Dr Roland Köhler, MD, MedDir/LTCol (res) MC, Medical Office, German Armed Forces; Dr Paul C.