Fine hand movements require the synergistic contraction of intrinsic and extrinsic muscles to achieve them. In this paper, a Finite Element Digital Human Hand Model (FE-DHHM) containing solid tendons ...and ligaments and driven by the Muscle-Tendon Junction (MTJ) displacements of FDS, FDP and ED measured by ultrasound imaging was developed. The synergistic contraction of these muscles during the finger flexion movements was analyzed by simulating five sets of finger flexion movements. The results showed that the FDS and FDP contracted together to provide power during the flexion movements, while the ED acted as an antagonist. The peak stresses of the FDS, FDP and ED were all at the joints. In the flexion without resistance, the FDS provided the main driving force, and the FDS and FDP alternated in a "plateau" of muscle force. In the flexion with resistance, the muscle forces of FDS, FDP, and ED were all positively correlated with fingertip forces. The FDS still provided the main driving force, but the stress maxima occurred in the FDP at the DIP joint.
Fine hand movements require the synergistic contraction of intrinsic and extrinsic muscles to achieve them. In this paper, a Finite Element Digital Human Hand Model (FE-DHHM) containing solid tendons ...and ligaments and driven by the Muscle-Tendon Junction (MTJ) displacements of FDS, FDP and ED measured by ultrasound imaging was developed. The synergistic contraction of these muscles during the finger flexion movements was analyzed by simulating five sets of finger flexion movements. The results showed that the FDS and FDP contracted together to provide power during the flexion movements, while the ED acted as an antagonist. The peak stresses of the FDS, FDP and ED were all at the joints. In the flexion without resistance, the FDS provided the main driving force, and the FDS and FDP alternated in a "plateau" of muscle force. In the flexion with resistance, the muscle forces of FDS, FDP, and ED were all positively correlated with fingertip forces. The FDS still provided the main driving force, but the stress maxima occurred in the FDP at the DIP joint.
...nonreproductive swarming due to the influence of pathogens is increased, even in honey bee colonies maintained under the same conditions when the number of pathogens have to reach a certain ...threshold (Fig 1) 2,5,9,16,17. Fitness benefits can be gained when the preference for a healthy mate is associated with heritable resistance to and/or tolerance for parasites that will be passed to offspring 25. ...nonreproductive swarming can reduce the risk of infection by actively avoiding infected sexual partners, or habitat choice to escape parasites can result in niche expansion of insect hosts due to honey bee mating in the air 26. Genetic diversity in individuals related to foraging rates, food storage, and population growth led to boosts in fitness of the individuals, and when circumstances change, an organism’s first response is often behavioral, as in the evolution in adaptive behaviors. Because genetic diversity in a honey bee colony enhances its productivity and health, producing swarming is one of the ways to propagate its gene 33. ...it is worth mentioning that honey bees may use nonreproductive swarming as a possible strategy to separate pathogens from the colony, but how this population behavior has evolved to counteract pathogen attacks remains to be determined.
Although it had been reported that Israeli acute paralysis virus (IAPV) can cause systemic infection in honey bees, little is known about how it establishes this infection and results in the typical ...symptoms, paralysis and trembling. Here, we used our previously constructed IAPV infectious clone to investigate viral loads in different tissues of honey bees and further identify the relation between tissue tropism and paralytic symptoms. Our results showed that tracheae showed a greater concentration of viral abundance than other tissues. The abundance of viral protein in the tracheae was positively associated with viral titers, and was further confirmed by immunological and ultrastructural evidence. Furthermore, higher viral loads in tracheae induced remarkable down-regulation of succinate dehydrogenase and cytochrome c oxidase genes, and progressed to causing respiratory failure of honey bees, resulting in the appearance of typical symptoms, paralysis and body trembling. Our results showed that paralysis symptoms or trembling was actually to mitigate tachypnea induced by IAPV infection due to the impairment of honey bee tracheae, and revealed a direct causal link between paralysis symptoms and tissue tropism. These findings provide new insights into the understanding of the underlying mechanism of paralysis symptoms of honey bees after viral infection and have implications for viral disease prevention and specific therapeutics in practice.
Honey bee viruses are one of the most important pathogens that have contributed to the decrease in honey bee colony health. To analyze the infection dynamics of honey bee viruses, quantification of ...viral gene expression by RT-qPCR is necessary. However, suitable reference genes have not been reported from viral and RNAi studies of honey bee. Here, we evaluated the expression of 11 common reference genes (
ache
2,
rps
18, β
-actin
,
tbp
,
tif
,
rpl
32,
gadph
,
ubc
, α
-tubulin
,
rpl14
, and
rpsa
) from
Apis mellifera
(Am) and
Apis cerana
(Ac) under Israeli acute paralysis virus (IAPV), chronic bee paralysis virus (CBPV), and Chinese sacbrood virus (CSBV) infection as well as dsRNA-PGRP-SA treatment, and we confirmed their validation by evaluating the levels of the
defensin 1
and prophenoloxidase (
ppo
) genes during viral infection. Our results showed that the expression of selected genes varied under different viral infections.
ache
2,
rps
18, β
-actin
,
tbp
, and
tif
can be used to normalize expression levels in
Apis mellifera
under IAPV infection, while the combination of
actin
and
tif
is suitable for CBPV-infected experiments. The combination of
rpl
14,
tif
,
rpsa
,
ubc
, and
ache
2 as well as more reference genes is suitable for CSBV treatment in
Apis cerana
.
Rpl
14,
tif
,
rps
18,
ubc
, and α
-tubulin
were the most stable reference genes under dsRNA treatment in
Apis mellifera
. Furthermore, the geNorm and NormFinder algorithms showed that
tif
was the best suitable reference gene for these four treatments. This study screened and validated suitable reference genes for the quantification of viral levels in honey bee, as well as for RNAi experiments.
Honey bee viruses are associated with honey bee colony decline. Israeli acute paralysis virus (IAPV) is considered to have a strong impact on honey bee survival. Phylogenetic analysis of the viral ...genomes from several regions of the world showed that various IAPV lineages had substantial differences in virulence. Chronic bee paralysis virus (CBPV), another important honey bee virus, can induce two significantly different symptoms. However, the infection characteristics and pathogenesis of IAPV and CBPV have not been completely elucidated. Here, we constructed infectious clones of IAPV and CBPV using a universal vector to provide a basis for studying their replication and pathogenesis. Infectious IAPV and CBPV were rescued from molecular clones of IAPV and CBPV genomes, respectively, that induced typical paralysis symptoms. The replication levels and expression proteins of IAPV and CBPV in progeny virus production were confirmed by qPCR and Western blot. Our results will allow further dissection of the role of each gene in the context of viral infection while helping to study viral pathogenesis and develop antiviral drugs using reverse genetics systems.
and some
species are the main pathogenic fungi of honey bee, and
is the pathogen of chalkbrood disease. However, the infection mechanism of them is incompletely known and it is still unclear whether ...other factors impact their pathogenesis. In this study,
were obtained from the chalkbrood bee samples for the first time. Our results showed that
could promote the accumulation of the spores of
. Pathogenicity test found that inoculation of the spores of the two fungi alone or their combination could induce disease characterization of chalkbrood and stonebrood but the extent was less than those in field. To further identify other pathogens impacted the pathogenesis, we found several honey bee viruses presented in the pathogenic fungi
and
, which were different from previous reported. Our results indicated that acute bee paralysis virus (ABPV) and chronic bee paralysis virus (CBPV) could replicate in these two fungi and increased in titer with the going of cultivation time. In addition, CBPV could not only transmit vertically to the next generation by spores, but also spread horizontally to different fungi through hyphal anastomosis. These results suggested that the honey bee chalkbrood contained the other pathogenic fungi besides
, the interactions between different pathogens of chalkbrood microbial communities may influence the prevalence of chalkbrood. Moreover, the discovery of honey bee viruses and their transmission mode in these two fungi enhanced the potential of exploring fungi virus as valuable factors that cause fungal disease outbreak.
Sacbrood is an infectious disease of the honey bee caused by Scbrood virus (SBV) which belongs to the family Iflaviridae and is especially lethal for Asian honeybee Apis cerana. Chinese Sacbrood ...virus (CSBV) is a geographic strain of SBV. Currently, there is a lack of an effective antiviral agent for controlling CSBV infection in honey bees.
Here, we explored the antiviral effect of a Chinese medicinal herb Radix isatidis on CSBV infection in A. cerana by inoculating the 3rd instar larvae with purified CSBV and treating the infected bee larvae with R. isatidis extract at the same time. The growth, development, and survival of larvae between the control and treatment groups were compared. The CSBV copy number at the 4th instar, 5th instar, and 6th instar larvae was measured by the absolute quantification PCR method.
Bioassays revealed that R. isatidis extract significantly inhibited the replication of CSBV, mitigated the impacts of CSBV on larval growth and development, reduced the mortality of CSBV-infected A. cerana larvae, and modulated the expression of immune transcripts in infected bees.
Although the mechanism underlying the inhibition of CSBV replication by the medicine plant will require further investigation, this study demonstrated the antiviral activity of R. isatidis extract and provides a potential strategy for controlling SBV infection in honey bees.
•The Bama minipig can be a model to study pathological scar.•Pressure improves wound healing and alleviates scar formation.•Pressure inhibits IGF-1/IGF-1R signal pathway.•Pressure suppresses collagen ...expression.
Pressure therapy has been widely used in clinical practice for the prevention or treatment of hypertrophic scars resulted from aberrations in wound healing. However, the precise molecular mechanisms of this process are only partially understood. In the present study, we established a Bama minipig model to observe the effect of pressure intervention on wound healing and scar formation. Transcriptome sequencing was performed to analyze the gene expression profiles in the injured and pressure-treated tissues. Furthermore, expression of the critical factors associated with IGF-1/IGF-1R pathways including PI3K/AKT and MEK/ERK and collagens were further analyzed by quantitative polymerase chain reaction (q-PCR) and Western blot. We observed that the mRNA expression of IGF-1 and IGF-1R were down-regulated in the pressure treated groups. Following pressure intervention, the trend in expression of PI3K/AKT decreased, whereas that of MEK/ERK expression increased, when quantified by q-PCR. Moreover, the level of PI3K protein expression decreased significantly after pressure treatment for one month but there was no significant difference in AKT protein expression. Interestingly, the trend in MEK/ERK protein expression was opposite to that indicated by q-PCR analysis. Furthermore, collagen I and III mRNA clearly declined after one month pressure treatment. Taken together, these results indicated that pressure intervention alleviated scar formation may via inhibiting the IGF-1/IGF-1R signaling pathway and collagen expression in the Bama minipig model.
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