These data provide information about population growth, which is useful in monitoring and for predicting the expansion of this non-native species, as well as giving

an opportunity to compare the different populations of the same species inhabiting different geographical locations. Individuals of the North American Harris mud crab were collected Selleckchem CH5424802 between 2006 and 2010 from the Gulf of Gdańsk at randomly chosen sampling points (Hegele-Drywa & Normant 2014) (Figure 1). Samples were taken with a bottom dredge (33 × 66 cm, mesh size 0.5 × 0.5 cm) from the r/v ‘Oceanograf 2’, at 129 randomly chosen sampling points located at depths from 5 to 60 m from 2006 to 2010 (Table 1). The single dredging time was 5 min at a vessel speed of 1.5 knots. CPUE was estimated for four people during five hours. Specimens were hand-sorted from the sampled material and frozen (–20°C) directly after collection. In the laboratory, the crabs were sexed on the basis of abdominal structure and pleopod

Ibrutinib in vitro shape (De Man 1892). Furthermore, during examination crabs were analysed for evidence of the external form of the rhizocephalan Loxothylacus panopaei ( Gissler 1884). Specimens with a carapace width < 4.4 mm were classified as juveniles ( Turoboyski 1973), and females with eggs attached to the pleopods were classified as ovigerous. Carapace width (CW) and length (CL) and major chela length (CHL) and height (CHH) were measured (± 0.01 mm) with slide calipers. Moreover, while these Sclareol measurements were being made, right vs. left claw dominance was determined. Growth ratios for the independent variable (CW) and dependent variables (CL, CHL) were determined by using the logarithmic transformation (log y = log a + b log x) and the function y = axb, where x is the independent variable (CW), y is the dependent variable, a is the intercept (value of y when x = 0), and b the slope

of the regression line. The value of b indicates the growth patterns of the variables: b = 1 (isometry), b < 1 (negative allometry), b > 1 (positive allometry) (Hartnoll 1982). The statistical significance of b was tested using Student’s t-test. After surface water had been blotted off the individual animals with soft tissue paper, their wet weight was measured with an accuracy of ± 0.001 g. They were then dried at 55°C to constant weight and reweighed. The crabs were divided into 2 mm carapace width classes. Some of the crabs were incomplete (e.g. with a missing walking leg or chela); therefore fewer specimens were used in a particular analysis (e.g. the carapace width-wet weight relationship) than the total number of specimens collected. Fulton’s condition factor (K) was calculated for each individual according to the equation given by Nash et al. (2006): K=100×WW/bCW,K=100×WW/CWb,where WW is the wet weight of an individual [g], CW is the carapace width [mm] and b is the regression coefficient of the carapace width-wet weight relationship. Analyses were carried out using the STATISTICA 8.0 PL program.

Slides were evaluated http://www.selleckchem.com/products/BKM-120.html using a Leica DMR upright microscope equipped for epifluorescence microscopy. ST sections were stained for TH immunoreactivity (IR) using nickel enhancement and slides were scanned as 600 dpi, 8 bit grayscale tiff images

using a CanoScan8400F flatbed scanner with automatic settings disabled. One section at the level of the anterior commissure (−0.26 mm from Bregma) was chosen from each brain for fiber density measurement. Using Fiji software (http://imageJ.nih.gov/ij), each ST was outlined using the freehand tool, processed to correct for background and brightness, converted to a binary image and the number of pixels in the ST determined as a measure of TH-IR fiber density. ST fiber density data are expressed as a percentage of injected vs control ST for each treatment group. Sections of SN were stained for TH-IR without nickel enhancement. For the dose response study, the number of TH-IR neurons was counted in both injected and control SNs in one section from each brain at the level of the medial terminal nucleus accessory optic tract (−5.3 mm from Bregma) using Neurolucida software (Micro Bright Field Biosciences). Protein Tyrosine Kinase inhibitor For the efficacy study, unbiased stereology was used to determine the total number of TH-IR neurons in each SN. Seven sections at similar anterior to posterior levels were chosen throughout

the anterior-posterior extent of the SN in every brain. The number of TH-IR cells was counted in injected and control SN using StereoInvestigator™ software (Micro Bright Field Biosciences). Parameters were as follows: grid size (80×80), frame size (175×175), guard zones (3 μm), optical dissector height (10 μm). The Gundersen coefficient of error was ≤0.07 for TH neuronal counts in the

control SN and ≤0.11 for tuclazepam TH neuronal counts in experimental SN. For both counting methods, only large TH-IR neurons (greater than ~15 μm in diameter) were counted to avoid counting interneurons or dying neurons. Histology images were collected using a Retiga 4000R digital camera on a Leica DMR upright microscope. Adobe Photoshop CS5 was used to compile multi-photo plate figures. Data were analyzed using Prism software. Kruskal–Wallis one-way ANOVAs followed by Dunn’s post hoc tests were used to compare treatment groups for forelimb behavior analysis. All other data were analyzed using a parametric one-way ANOVA followed by Tukey’s post hoc tests. Statistically significant differences were set at p≤0.05. Data are expressed as mean±SEM. This study was supported by the Department of Defense Neurotoxicology Program (NO06079001) and NIH grants (NS31957 and NS054989 to M.C.B. and T32 NS041234 to C.E.K.), the Harry F. and Elaine M. Chaddick Foundation and the Medical Research Institute Council of Ann and Robert H. Lurie Children’s Hospital of Chicago. The University of Pennsylvania Viral Vector Core is acknowledged for AAV production. The technical assistance of Jianping Xie and Brian Corstange (Ann and Robert H.

The zeros and signs of δ¯ρFB actually tend to coincide with those of ρ¯0zz (not shown) because δρ≈-aδT+bδS, the vertical gradients of a   and b   are small, and hence δρδρ itself approximately obeys (7). Furthermore, the amplitudes in corresponding left and right panels are similar, although the actual anomaly tends to be somewhat weaker than that computed from (8), indicating that the growth of the anomalies has reduced below a linear trend within a year, owing to the onset of the adjustment processes discussed in Section 3.2.3. The exception is within 3° of the southern and northern boundaries where density anomalies

are small and the contours of the total density field are nearly horizontal (top panels), a consequence of find more the restoration of temperature and salinity toward prescribed values in those regions (Section 2.1). If density depends only on temperature, only on salinity, or if T   and S   have the same vertical structure (and the vertical gradients of ∂ρ/∂T∂ρ/∂T and ∂ρ/∂S∂ρ/∂S are negligible), a diffusion anomaly, δκbδκb, will only generate a dynamical anomaly, that is, it will shift isopycnals vertically with no change in spiciness. In the real ocean

AZD2281 nmr (and in our control run), however, T   and S   have different structures, and δκbδκb generates both spiciness and dynamical anomalies ( A). Fig. 4b illustrates the generation of both anomaly types in Solution FB, comparing δTFBδTFB (top-left) to its parts due GPX6 to dynamics δ′TFBδ′TFB (middle-left) and spiciness δ″TFBδ″TFB (bottom-left) during year 1. The pattern of the total temperature anomaly δTFBδTFB is very similar to that of δρFBδρFB in Fig. 4a (top-left panel) and it is largely explained by δ′TFBδ′TFB, especially in the tropics. In the subtropics, however, δ″TFBδ″TFB is significant because there are prominent salinity signals associated with subsurface waters, namely, high-salinity North Pacific Tropical Water ( Tsuchiya, 1968 and Suga et al., 2000, and references therein) and South Pacific Subtropical Lower Water ( Wyrtki, 1962) overlying

deeper, lower-salinity waters ( Wyrtki, 1962 and Talley, 1985). Fig. 4b also plots temperature anomalies where (7) is assumed to hold individually for both temperature and salinity (right panels). They show that the general patterns of all the anomaly fields in Solution FB are well predicted by the one-dimensional model. After the initial and local responses, solutions adjust toward a new equilibrium state through wave radiation, advection, and mixing. Locally-forced dynamical anomalies are associated with an unbalanced pressure field that excites baroclinic waves. In contrast, spiciness anomalies do not affect pressure (they are a passive tracer), and hence respond only to advection and mixing.

Opis badania powinien obejmować: wielkość (długość), echostrukturę i echogeniczność nerek, ewentualne poszerzenie układu kielichowo-miedniczkowego (miedniczka i kielichy), szerokość moczowodów oraz wielkość i grubość ścian pęcherza moczowego. Poród dziecka, u którego podejrzewa się poważną wadę wrodzoną układu moczowego, powinien odbywać się w ośrodku referencyjnym III stopnia, zapewniającym możliwość konsultacji urologa i nefrologa dziecięcego. Zaleca

się, by wszystkie dzieci z podejrzeniem prenatalnym wady układu moczowego miały wykonane Epigenetics inhibitor badanie ultrasonograficzne jamy brzusznej w pierwszych dobach życia (doba 1.–7.). O terminie badania decyduje stan dziecka i rodzaj podejrzewanej wady (badanie pilne w 1.–2. dobie, a badanie planowe w 3.–7. dobie). Do ustalenia postępowania zalecane jest kolejne badanie ultrasonograficzne jamy brzusznej, które powinno zostać wykonane w terminie 4.–6. tygodni od pierwszego. Do ustalenia właściwego postępowania z noworodkiem niezbędna jest możliwość analizy: ilości wód płodowych, prenatalnej wielkości nerek i szerokości dróg moczowych, stanu klinicznego noworodka (skala Apgar) i wielkości diurezy po porodzie. Poród dziecka

z podejrzeniem poważnej wady wrodzonej układu moczowego (skąpowodzie, brak miąższu obu nerek, zastawki cewki tylnej) powinien odbywać się w ośrodku Selleck BMS-907351 referencyjnym zapewniającym intensywną opiekę okołoporodową. Należy wykonać badanie USG w pierwszej dobie życia, monitorować diurezę poprzez założenie cewnika do pęcherza moczowego, włączyć profilaktykę zakażeń układu moczowego oraz ocenić czynność nerek poprzez pomiar diurezy godzinowej, a także pomiar stężenia mocznika i kreatyniny w surowicy (z uwzględnieniem wartości tych wskaźników u matki). Konsultacja urologa i nefrologa powinna odbyć Anidulafungin (LY303366) się w trybie pilnym (Ryc. 1). Planowa diagnostyka u noworodka w dobrym stanie ogólnym obejmuje badanie ultrasonograficzne w 3.–7. dobie po urodzeniu, co pozwala uniknąć

wyników fałszywie ujemnych spowodowanych przejściowym, fizjologicznym, gorszym nawodnieniem dziecka w 1.–2. dobie życia 2., 3., 4. and 5.. Jeśli w prenatalnym badaniu USG rozpoznano izolowane jedno-lub obustronne poszerzenie układu kielichowo-miedniczkowego (UKM), nie istnieje podejrzenie obecności wady złożonej. Poród dziecka i wstępna postnatalna weryfikacja wady mogą być przeprowadzone w szpitalu rejonowym. Za istotne poszerzenie UKM, wymagające monitorowania, uznaje się poszerzenie miedniczki nerkowej w projekcji A-P powyżej 5 mm w 3.–7. dobie życia i 10 mm w 4.–6. tygodniu lub później. W przypadku izolowanego, niepowikłanego, jednolub obustronnego poszerzenia UKM nie ma wskazań do wykonania cystografii mikcyjnej. Przyczyną poszerzenia UKM u płodu jest najczęściej przeszkoda zlokalizowana na wysokości połączenia miedniczkowo-moczowodowego.

Four examples of optimal wavelength relationships, one for each biogeochemical quantity, are given in Table 2. In the case of SPM and POC estimates, the best results are achieved when values of bbp are used selleck kinase inhibitor for the wavelength 420 nm (see lines 1 and 2 in Table 2). But the statistical parameters

characterising these two new relationships are very similar to those given for the two formulas presented earlier ( (1) and (2)) which make use of approximated values of bbp(443). No significant improvement is achieved in these two cases (compare the statistical parameters shown in Table 2 and Table 1). A small but noticeable improvement can be found for the statistical relationship between POC and an(488) (see line 3 in Table 2, and Figure 5a): equation(6) POC=1.35(an(488))0.923.POC=1.35an4880.923. In this case, when we compare it to the equation (3) MK-2206 datasheet presented earlier, there is a decrease in the standard error factor X from 1.59 to 1.55. But the largest possible improvement in favour of a formula making use of the optimal wavelength is obtainable (and this is also in agreement with common physical intuition) for a formula for estimating Chl a based on values of an(676), i.e. values at the red peak of that pigment absorption spectrum (see line 4 in Table 2, and Figure 5b): equation(7) Chla=45.6an6760.854.

In this case, when we compare the standard error factor X to equation (4) presented earlier, the improvement in its value is the largest (i.e. the value of X decreases from 1.54 to 1.35). But the values of all the statistical parameters obtained in that particular case have to be treated with extra caution. The values of coefficient an(676) measured with the AC-9 instrument are spectrally located close to the 715 nm band, at which, according to the absorption measurement correction Nabilone methodology applied in this work (the so-called proportional method, see the Methods section), the whole of the measured signal was assumed to have been caused by light scattering, and was consequently

subtracted to make an(715) equal to 0. Although this methodology has been widely used by many oceanographers, it is known to be an imperfect simplification (see e.g. the discussion in the paper by McKee et al. (2008)). In situations where the assumption that absorption by particles in water of the 715 nm band is negligible does not hold, the resultant corrected absorption coefficients an could be encumbered with a certain error, especially for bands lying spectrally close to the band used for correction. As a result of this, the corrected values of an(676) in our case may represent the height of the 676 nm absorption peak above the true but unknown value of absorption at 715 nm rather than the real absolute value of absorption at 676 nm. The other fact which should also be taken into account, and is obviously not analysed here, is that apart from the supposed statistical attractiveness of the Chl a vs.

This was a 12-month, phase III, multicenter, randomized, double-blind, parallel group, active comparator controlled study in Japanese patients with involutional osteoporosis. Diagnosis of osteoporosis was based on the presence or absence of fragility fracture and BMD measurements specified in the “Guideline for the Diagnosis of Primary Osteoporosis (2000 Revised Version)” established by the Japanese Society for Bone and Mineral Research GSI-IX in vitro [20] and [21]. Individuals eligible for this study were ambulatory Japanese male and female subjects aged ≥ 50 years who were diagnosed with osteoporosis, based on the criteria for primary osteoporosis of the Japanese Society for Bone and

Mineral Research [20] and [21]. Primary osteoporosis was defined by the presence of a fragility fracture and BMD < 80% of the ‘young adult mean’ (20 to 44 years of age), or BMD < 70% of the ‘young adult mean’ in the absence of a detectable fragility fracture [21]. In the case of female subjects, ≥ 2 years must have passed since menopause.

The main exclusion criteria were factors which affect 3-Methyladenine mouse efficacy evaluation; secondary osteoporosis and any other disease causing decreased bone mass or affecting lumbar spine BMD (including severe scoliosis of the spine, fracture or severe deformation in any of the L2–L4 lumbar vertebrae, or a spinal X-ray image suggesting severe bone sclerosis [calcification] in any of the L2–L4 lumbar vertebrae); Morin Hydrate administration of bisphosphonate within 24 weeks before the first dose of the study

drug; administration of any drug affecting bone metabolism such as SERMs, vitamin D3 and vitamin K2 preparations, and calcitonin analogs, etc. within 8 weeks before the first dose of the study drug. In addition, any subject judged by the attending physician to be unsuitable to participate in the study was also excluded. The study was performed at 60 study sites in Japan between February 2010 and August 2011 in accordance with the ethical principles set out in the Declaration of Helsinki and the ICH Harmonized Tripartite Guideline for Good Clinical Practice, and was approved by the Institutional Review Boards at each study site in line with local regulations. Prior to study registration, all subjects were given a full explanation of the study procedures and provided written informed consent. Subjects fulfilling the inclusion/exclusion criteria were eligible for the study and were randomized (in a ratio of 1:1) to receive risedronate 75 mg once-monthly or risedronate 2.5 mg once-daily. Matching 2.5 mg and 75 mg placebo tablets were administered to maintain double blindness throughout the study. Subjects were instructed to take a single 75 mg risedronate tablet or 75 mg placebo tablet on the same calendar day each month and a single 2.5 mg risedronate tablet or 2.5 mg placebo tablet at the designated time on every day.

The supernatants were collected for the assays. Activation of caspase-9 is based on hydrolysis of the substrate n-Acetyl-Leu-Glu-His-Asp7-amido-4-trifluoromethylcoumarin

(Ac-LEHD-AFC) by caspase-9, resulting in the release of fluorescent 7-amino-4-trifluromethyl coumarin (AFC) moiety, while hydrolysis of the peptide substrate acetyl-Asp-Glu-Val-Asp-7-amido-4-methylcoumarin (Ac-DEVD-AMC) by caspase-3, resulted in the release of the fluorescent 7-amino-4-methylcoumarin (AMC) moiety. Reaction were performed selleck chemicals in buffer containing supernatant proteins (50 μg/sample for caspase-9 and 25 μg/Sample for caspase-3) and caspase substrates, at 37 °C for 2 h, followed by fluorimetric detection using the excitation and emission wavelengths of 400/505 nm and 360/460 nm for caspase-9 and caspase-3, respectively. The experimental data were evaluated using the analysis of variance (ANOVA), followed by the Dunnet test for the

comparison of the various treated groups with their controls, using the GraphPrism program, version 5.1 for Windows. The results were considered statistically significant at p < 0.05. The results showed that the congener BDE-99 inhibited cell proliferation after 24 and 48 h selleck chemicals llc of incubation, showing significant effects at the higher concentrations tested (18.22 ± 6.42% and 41.77 ± 10.5% for 10 μM and 25 μM, respectively) after 24 h of exposure. A significant effect was observed for concentrations as low as 0.5 μM when the cells were exposed to the compound for 48 h (Fig. 1). Moreover, it was also demonstrated that the congener BDE-99 was able to induce a decrease in cell viability during both incubation periods for almost all the concentrations that lead to an inhibition of HepG2 cell proliferation (Fig. 2). These results demonstrated that there is a correlation between the effects observed in the first two experiments. Fig. 3 shows

Rucaparib manufacturer the effect of BDE-99 on the mitochondrial membrane potential (MMP). The MMP also changed after exposure to 10 and 25 μM of the compound for 24 h. This effect was intensified after 48 h of incubation, showing significant effects in concentrations as low as 0.5 μM. Similar results to those of the MMP assay were observed in the ROS accumulation test. Fig. 4 shows a significant increase in ROS accumulation after 24 h of incubation with BDE-99 at the highest concentration tested (25 μM). However when the effect was evaluated for 48 h, the exposure to 5 μM of the compound was sufficient to significantly increase ROS accumulation in the HepG2 cells. To better understand the mechanism by which BDE-99 induces cell death, we evaluated the exposure of phosphatidyl serine on the outer cell membrane by assessing the FITC-annexin-V positive cells. Fig.

Clearly

the Vallee Professorship was extremely valuable for my scientific career. At the core of the Vallee Visiting Professor program is its collaborative mentality. Academic-social interactions play a key role in generating new ideas and are thus a central focus for VVPs. Such was the case for Torsten Wiesel, who came in May 2010, to renew contact with the Department of Neurobiology, where he had previously been www.selleckchem.com/products/r428.html a member for twenty years, serving as chair for ten of them. Having left his research career for various administrative roles, he was interested to get an insider’s view of his old department. In Torsten’s words, my experience as a Vallee Visiting Professor was intellectually rich and wonderful. I met with nearly the entire faculty of the department individually, which turned out to be a

very enriching and enjoyable experience. The faculty members described their research programs, followed by intense and detailed discussions about various aspects of their work. It was not until later, when attending a dinner for Torsten – the Foundation hosts a festive dinner near the end of each visit both to celebrate the Vallee Visiting Professor, and to recognize the contributions of his/her colleagues and friends during the visit – that it was learnt of the intangible consequences of Torsten’s visit that had widely impacted his host department. Senior members of the Department of Neurobiology said that Torsten’s presence DNA Damage inhibitor in the department had incited a palpable energy that stirred ideas and renewed drive not just among principal investigators, but also throughout the ranks in their laboratories. When Malcolm Green came in 2004 to Jeremy Knowles’ laboratory in the Department of Chemistry, the visit provided a much-needed opportunity

to think about my future research program. But, apart from check working on research, Malcolm established or renewed many friendships, often over dinner at Jeremy and Janey Knowles’ home, with prominent figures such as Alan Davison, Dick Schrock, Dietmar Seyferth, Dan Nocera, Steve Lippard, Dick Holm, George Whitesides, John Deutsch, and Samuel P. Huntington. Likewise, Jesper Haeggström, who visited the lab of Charles Serhan at Brigham and Women’s Hospital, recalls being particularly stimulated by all the informal meetings and discussions with distinguished colleagues both inside and outside my own immediate fields of interest. I remember spending one morning in K. Frank Austen’s laboratory, sharing thoughts on intracellular lipid receptors with Peter Weller, and learning the latest new developments regarding in vivo imaging from Ulrich von Andrian. In addition to these meetings, being in Charles Serhan’s lab allowed ample opportunities to interact with all members of a world-leading team in the field of lipid mediator research.

Nobuo showed us impressive slides about his work on sea snake venoms. I remember a slide where he was holding a large Laticauda snake. He assured us that the snake was alive. He topped his talk when he mentioned that a sea snake, he was keeping as a pet in his lab, had escaped from the aquarium. When searching for the snake he

finally found it under his desk. Horror-stricken we were and knowing Tariquidar the high lethality of the snake’s venom we asked him, what kind of precautions he usually made. “Nothing” he replied, “because they never bite”. I kept this remark in my mind, but was still hesitating when I caught my first sea snake many years later in Palau, Micronesia. Nobuo Tamiya died on January 19, 2011 at the age of 88. Nobuo Tamiya was born on July 7, 1922 in Tokyo. He studied chemistry at the Tokyo Imperial University and after to Bachelor of Science 1944, he entered the Graduate School of the University where he worked shortly as assistant professor in the Department of Biochemistry. Soon he was drafted for military service to join the marine student reserves. Nobuo rarely spoke about this time when he saw so many of his fellow students senselessly sacrificing their life for the emperor and the country in the last months of the war. When the war was over, he returned to the University of Tokyo,

completed his thesis and received his PhD in November 1954. He was appointed associate professor learn more in the laboratory of Prof. Shiro Akabori, a famous protein chemist. Like many of the generation of scientists in post-war Japan he went overseas as postdoc and spent a year (1955–1956) in Hans Krebs’ lab, the Nobel laureate in medicine 1953, at the University of Oxford, England, and another year (1956–1957) in New York at the Columbia University in the lab of D. Rittenberg. These years certainly contributed to Nobuo’s attitude to welcome and care for international

contacts and cooperation. When he returned to Japan, he became professor at the Tokyo Medical and Dental University and in 1965 he moved to the Tohoku University in Sendai, where he was Professor at the Department of Chemistry till his retirement in 1985. In 1966 Nobuo and his coworker H. Arai published Alanine-glyoxylate transaminase a paper on the crystallization of erabutoxins a and b (Biochem. J. 99, 624–630), “short” (62 amino acids) neurotoxins from the venom of the sea krait Laticauda semifasciata, which specifically act on the acetylcholine receptor of the motor nerve endplate. It laid the basis for a series of studies such as on the immunological properties of snake venom neurotoxins (with André Ménez) and provided Barbara Low with the chance to determine the three-dimensional structure of erabutoxin b by x-ray diffraction analysis (Proc.Natl. Acad. Sci. USA 73, 2991–2994, 1976).

anomala

and may be treated as a plea for more future studies on the life cycle and other biological characteristics of this species, which would enable its mass production for aquaculture. This study aims to follow up the monthly variation of the biometric measurements of the nereid in question, as well as the sex ratio, fecundity, egg ripeness and spawning season in relation to the environmental conditions along the Alexandria coast. Two sites characterised by abundant P. anomala were selected along the Alexandria coast, namely, Abu-Qir and El-Mex ( Figure 1). Abu Qir is an exposed site on the western edge of Abu-Qir Bay east of Alexandria City, with a bottom containing a chain of natural rocks covered by a rich algal flora. El Mex is also an exposed rocky area Obeticholic Acid in vivo on the western part of the Alexandria coast; it is directly

affected by industrial, agricultural and sewage discharges. Salinity, temperature, pH, dissolved oxygen (DO) and biochemical oxygen demand (BOD) were measured concurrently with polychaete collection. Both water temperature and pH were measured in the field using a digital portable pH − °C meter (HANNA 10pH). Salinity was determined with a calibrated salinometer (Beckman, Model RS-7C). DO and BOD were determined according to the Winkler method (Strickland & Parsons 1972). The P. anomala worms were collected monthly by scraping the benthos from Buparlisib rocky substrates; the samples were placed in 5 litre plastic jars. The worms were sorted, counted and preserved in 4% buffered formalin for the biological observations and finally preserved in 70% ethanol. Several biometric parameters were measured for each monthly number of worms, namely the total length (TL), length to the 6th segment (L6S), body

width at the 6th segment (W6S), prostomium length (PL) and prostomium width (PW). In order to minimise the formalin effect, the biometric measurements were done directly after sorting. The relationships between the biometric parameters were assessed by using regression and Pearson moment correlation analyses. The length-weight relationship was determined according to the allometric equation W = aLb (Hile, 1936 and Bechamn, 1948), where ‘W’ – total body wet weight [g], ‘L’ clonidine – body length [cm], ‘a’ – a constant and ‘b’ – the growth coefficient. Numerous worms were dissected partially to define the sex and to collect eggs from females. The diameters of about 40 oocytes were measured monthly using an eye-piece micrometer; the mean diameter was calculated. Fecundity expressed as the number of eggs per female was found by counting all the ripe oocytes in the coelom of fully mature, intact, i.e. uninjured, females. Males were identified by the presence of sperm plates or sperm aggregates in the coelomic fluid, while worms without sexual products were considered immature.