[Community structure of macrozoobenthos and its relationship with environmental factors in Sanmen Bay, Zhejiang, China]. / ä¸‰é—¨æ¹¾å¤§åž‹åº•æ –åŠ¨ç‰©ç¾¤è½ç»“æž„åŠå ¶ä¸ŽçŽ¯å¢ƒå› å­çš„å ³ç³».

To understand the status and dynamics of macrozoobenthos community in Sanmen Bay, we collected benthos samples by Agassiz trawl in November 2015, and February, May and August in 2016. The results showed that: 1) A total of 119 macrozoobenthos species were recorded, with main groups of fishes, crustaceans and molluscs, accounting for 79% of the total number of species. 2) The dominant species of macrozoobenthos throughout the year were Leptochela gracilis, Hyperacanthomysis longirostris and Amblychaeturichthys hexanema. The identity of dominant species changed significantly in different seasons. 3) The annual average biomass and density were 0.025 g·m-2 and 0.07 ind·m-2, respectively. 4) The Shannon's diversity index of macrozoobenthos in Sanmen Bay varied from 2.21 to 3.18, the Margalef's species richness index varied from 3.25 to 3.78, and the Pielou's evenness index varied from 0.53 to 0.79. Results from abundance-biomass curve analysis showed that the community was moderately disturbed in spring and winter, and slightly disturbed in summer and autumn. Results from Canonical correspondence analysis showed that water depth, temperature, salinity, and pH were the most important environmental factors affecting macrozoobenthos community.

[Feeding habits of Trachurus japonicus in the East China Sea].

A total of 453 Trachurus japonicus specimens with a fork length (FL) of 46-250 mm were sampled in the seasonal light seine net surveys in the East China Sea in May, August, and November, 2008 and in February, 2009. The stomach contents of the specimens were analyzed, and the seasonal and ontogenetic variations in the feeding habits of the T. japonicus were examined by the Kruskal-Wallis test, chi-squared test, and cluster analysis. There were 124 prey species (including not identified) ingested by the T. japonicus, among which, planktonic crustaceans and small-scale marine fish made up the dominant prey groups. According to the percentage index of relative importance (IRI%), Bregmaceros macclellandi was the most dominant prey, accounting for 39.2%, followed by Macrura mysis larva (18.4%), brachyura zoea larva (7.6%), and Euphausia pacifica (6.6%). The feeding intensity of the T. japonicus varied significantly with its FL and season, being the highest for the T. japonicus with a FL of 140-159 mm, higher for the T. japonicus juveniles with a FL of 45-99 mm, while lower for the T. japonicus of other size classes, and the highest in spring and the lowest in winter. Cluster analysis revealed there was an abrupt change in the diet composition for the T. japonicus with a FL of about 100 mm FL. The average trophic level of the T. japonicus in four seasons was 3.51, indicating that the T. japonicus in the East China Sea was of low-level carnivores feeding on plankton and nekton.

Further evidence for involvement of a noncanonical function of uracil DNA glycosylase in class switch recombination.

Activation-induced cytidine deaminase (AID) introduces DNA cleavage in the Ig gene locus to initiate somatic hypermutation (SHM) and class switch recombination (CSR) in B cells. The DNA deamination model assumes that AID deaminates cytidine (C) on DNA and generates uridine (U), resulting in DNA cleavage after removal of U by uracil DNA glycosylase (UNG). Although UNG deficiency reduces CSR efficiency to one tenth, we reported that catalytically inactive mutants of UNG were fully proficient in CSR and that several mutants at noncatalytic sites lost CSR activity, indicating that enzymatic activity of UNG is not required for CSR. In this report we show that CSR activity by many UNG mutants critically depends on its N-terminal domain, irrespective of their enzymatic activities. Dissociation of the catalytic and CSR activity was also found in another UNG family member, SMUG1, and its mutants. We also show that Ugi, a specific peptide inhibitor of UNG, inhibits CSR without reducing DNA cleavage of the S (switch) region, confirming dispensability of UNG in DNA cleavage in CSR. It is therefore likely that UNG is involved in a repair step after DNA cleavage in CSR. Furthermore, requirement of the N terminus but not enzymatic activity of UNG mutants for CSR indicates that the UNG protein structure is critical. The present findings support our earlier proposal that CSR depends on a noncanonical function of the UNG protein (e.g., as a scaffold for repair enzymes) that might be required for the recombination reaction after DNA cleavage.

Prevention of paclitaxel-evoked painful peripheral neuropathy by acetyl-L-carnitine: effects on axonal mitochondria, sensory nerve fiber terminal arbors, and cutaneous Langerhans cells.

Prophylactic treatment with acetyl-L-carnitine (ALCAR) prevents the neuropathic pain syndrome that is evoked by the chemotherapeutic agent, paclitaxel. The paclitaxel-evoked pain syndrome is associated with degeneration of the intraepidermal terminal arbors of primary afferent neurons, with the activation of cutaneous Langerhans cells, and with an increased incidence of swollen and vacuolated axonal mitochondria in A-fibers and C-fibers. Previous work suggests that ALCAR is neuroprotective in other nerve injury models and that it improves mitochondrial dysfunction. Thus, we examined whether the prophylactic efficacy of ALCAR was associated with the prevention of intraepidermal terminal arbor degeneration, the inhibition of Langerhans cell activation, or the inhibition of swelling and vacuolation of axonal mitochondria. In animals with a confirmed ALCAR effect, we found no evidence of a neuroprotective effect on the paclitaxel-evoked degeneration of sensory terminal arbors or an inhibition of the paclitaxel-evoked activation of Langerhans cells. However, ALCAR treatment completely prevented the paclitaxel-evoked increase in the incidence of swollen and vacuolated C-fiber mitochondria, while having no effect on the paclitaxel-evoked changes in A-fiber mitochondria. Our results suggest that the efficacy of prophylactic ALCAR treatment against the paclitaxel-evoked pain may be related to a protective effect on C-fiber mitochondria.

Involvement of caspase cascade in capsaicin-induced apoptosis of dorsal root ganglion neurons.

Capsaicin induces apoptosis in some types of neurons, but the exact molecular mechanism remains unclear. In this study, capsaicin was systemically administrated in newborn rats and the dorsal root ganglion (DRG) neurons were examined for caspase-immunoreactivity. Capsaicin-induced neuronal apoptosis was revealed by TUNEL. TUNEL-positive neurons rapidly increased, reaching the peak at 24 h post-injection when 10.6% of DRG neurons were apoptotic. Neurons expressing immunoreactivity for activated caspases-9 and -3 concomitantly increased. At 24 h, 15.9% and 17.7% of DRG neurons exhibited immunoreactivity for caspase-9 and caspase-3, respectively. DNA fragmentation signal and caspase-immunoreactivity were detected in less than 0.5% of DRG neurons of vehicle control rats. The immunoreactivity and TUNEL-positivity returned to the vehicle control level by 120 h. Double label immunohistochemistry revealed co-expression of caspase-9 and DNA fragmentation or caspase-3 and DNA fragmentation. These results suggest that the caspase cascade is involved in the primary neuronal apoptosis induced by neurotoxin capsaicin.

Activation of the caspase cascade underlies the rat trigeminal primary neuronal apoptosis induced by neonatal capsaicin administration.

The systemic administration of capsaicin is known to cause a massive loss of sensory primary neurons in newborn rats. Here we examined the trigeminal ganglion neurons immunohistochemically for the possible induction of activated forms of caspases-9 and -3 following a subcutaneous injection of capsaicin in newborn rats. The DNA fragmentation signal was labeled by a TUNEL method. TUNEL-positive neurons were rare (< 0.5%) at 24 h after injection of the vehicle without capsaicin. After the capsaicin injection, TUNEL-positive neurons began to increase by 12 h, reached a peak at 24 h (11.4%), and returned to the control level by 120 h. Vehicle control levels of caspase- 9-immunoreactive (ir) and caspase-3-ir neurons were low (< 0.5%). Neonatal capsaicin administration induced caspase-9-immunoreactivity (ir) and -3-ir. The temporal distributions of caspase-9-ir and caspase-3-ir neurons were similar to those of TUNEL-positive neurons with peak expressions at 24 h of 13.2 and 11.1%, respectively. A double-stain analysis at 24 h post-injection indicated 72% of TUNEL-positive neurons were caspase-9-ir, and 70% caspase-3-ir. Conversely, 78 and 68% of caspase-9-ir and caspase-3-ir neurons, respectively, were TUNEL-positive. Comparison of two adjacent sections immunostained for the two different antigens revealed the co-expression of the two caspases. These results suggest that neonatal capsaicin triggers the caspase cascade and, thereby, induces trigeminal primary neuronal apoptosis.