Materials and Methods: A batch of newly hatched hybrid grouper fry (Epinephelus fuscoguttatus × Epinephelus lanceolatus) were followed from the larval stage to market size. Samples of the hybrid groupers, water, live feed, and artificial fish pellets were collected periodically from day 0 to 180 in the hybrid grouper hatchery. Reverse transcription-polymerase chain reaction (RT-PCR) and nested PCR amplifications were carried out on VNN-related sequences. The phylogenetic tree including the sampled causative agent of VNN was inferred from the coat protein genes from all known Betanodavirus species using Molecular Evolutionary Genetics Analysis (MEGA). Pearson's correlation coefficient values were calculated to determine the strength of the correlation between the presence of VNN in hybrid grouper samples and its associated risk factors.
Results: A total of 113 out of 146 pooled and individual samples, including hybrid grouper, water, and artificial fish pellet samples, demonstrated positive results in tests for the presence of VNN-associated viruses. The clinical signs of infection observed in the samples included darkened skin, deformation of the backbone, abdominal distension, skin lesions, and fin erosion. VNN was present throughout the life stages of the hybrid groupers, with the first detection occurring at day 10. VNN-associated risk factors included water temperature, dissolved oxygen content, salinity, ammonia level, fish size (adults more at risk than younger stages), and life stage (age). Detection of VNN-associated viruses in water samples demonstrated evidence of horizontal transmission of the disease. All the nucleotide sequences found in this study had high nucleotide identities of 88% to 100% to each other, striped jack nervous necrosis virus (SJNNV), and the reassortant strain red-spotted grouper NNV/SJNNV (RGNNV/SJNNV) isolate 430.2004 (GenBank accession number JN189932.1) (n=26). The phylogenetic analysis showed that quasispecies was present in each VNN-causing virus-positive sample, which differed based on the type of sample and life stage.
Conclusion: This study was the first to confirm the existence of a reassortant strain (RGNNV/SJNNV) in hybrid groupers from Malaysia and Southeast Asia. However, the association between the mode of transmission and the risk factors of this virus needs to be investigated further to understand the evolution and potential new host species of the reassortant strain.
MATERIALS AND METHODS: AuNPs are synthesized by Q-switched Nd:YAG laser ablation technique. Cutaneous wound are induced on 45 Sprague Dawley rats on its dorsal part and then randomly divided into three groups. One group serves as non-treatment group (GC) and another two groups are subjected to AuNPs with and without PBMT. About 808 nm diode laser with output power of 100 mW is used as a light source for PBMT. The treatment was carried out daily with exposure duration of 50 seconds and total fluence of 5 J/cm2 . Wound area is monitored for 9 consecutive days using a digital camera, and histological examination is performed at 3rd, 6th, and 9th day through hematoxylin and eosin stain as well as Masson's trichrome stain.
RESULTS: The group of rats subjected to AuNPs with PBMT shows significantly accelerated wound closure compared to other groups. Histological results indicate that AuNPs and PBMT group is more effective in stimulating angiogenesis and triggers inflammatory response at early stage.
CONCLUSION: The application of AuNPs in PBMT has potential to accelerate wound healing due to enhanced epithelialization, collagen deposition and fast vascularization. Lasers Surg. Med. 49:380-386, 2017. © 2016 Wiley Periodicals, Inc.
METHODS: DNA were extracted from formalin-fixed, paraffin-embedded tissues obtained from 33 CRC patients diagnosed between 2018 and 2019. Amplifications of codons 12 and 13 of KRAS were conducted using conventional polymerase chain reaction (PCR) followed by Sanger sequencing.
RESULTS: Mutations were identified in 36.4% (12/33) of patients, with G12D (50%) being the most frequent single-point mutation observed, followed by G12V (25%), G13D (16.7%), and G12S (8.3%). No correlation was found between mutant KRAS and location of the tumor, staging, and initial carcinoembryonic antigen (CEA) level.
CONCLUSION: Current analyses revealed that a significant proportion of CRC patients in the East Coast of Peninsular Malaysia have KRAS mutations, where this frequency is higher compared to those in the West Coast. The findings of this study would serve as a precursor for further research that explores KRAS mutational status and the profiling of other candidate genes among Malaysian CRC patients.
MATERIALS AND METHODS: This study utilized goldfish specimens sourced from Tulungagung, East Java, Indonesia. The experiment involved different concentration levels of benzalkonium chloride: (T1) 0 mg/L, (T2) 0.03 mg/L, (T3) 0.06 mg/L, (T4) 0.09 mg/L, and (T5) 0.12 mg/L. The research data were subjected to an analysis of variance for analysis. In cases where significant differences were observed, Duncan's test was conducted for color brightness, growth, and mortality data. Furthermore, if the gill histopathological data yielded significant differences, additional tests were applied (Kruskal-Wallis and Mann-Whitney test).
RESULTS: The findings of this study demonstrated significant differences (p < 0.05) in the level of color brightness, growth, gill histopathology, and mortality in goldfish in response to varying concentrations of benzalkonium chloride. The relationship between the length and weight of the goldfish was analyzed using regression coefficients (b values), which were determined as 4.86, -0.04, -0.2, 0.8, and -0.07, respectively. Notably, the brightness level in the T2 group exhibited positive color results with a hue value of 11.55°, while optimal growth was observed in the T4 group, as evidenced by b value of 0.8. The gill histopathological data showed significant differences (p < 0.05). The scoring of histopathological damage in the goldfish gills ranged from 0 to 10, with higher scores indicating more severe damage. The highest total score of 10 was observed in the T5 group exposed to a concentration of 0.12 mg/L, resulting in an 85% mortality rate. This indicates that benzalkonium chloride, with its toxic compounds, can disrupt the respiratory system of fish and lead to death.
CONCLUSION: The effects of benzalkonium chloride were evident even at a concentration of 0.03 mg/L. With increasing concentration, there was an increase in mortality rate, a decrease in growth, and a rise in histopathological damage to the gills. These findings highlight the negative impact of using conventional disinfectants on water and its organisms, emphasizing the need for further research on environmentally friendly alternatives.