Bark-stripping Behavior of Formosan Sambar (Rusa unicolor swinhoii) at Tataka, Yushan National Park in Taiwan.

The bark-stripping behavior of Formosan sambar, Rusa unicolor swinhoii, has become conspicuous in recent years in the Tataka area of Yushan National Park in Taiwan and a cause for concern to visitors and ecologists. We conducted a monthly survey of 537 tagged trees of 21 species and monitored the abundance of sambar using camera traps from October 2018 to January 2021, aiming to interpret possible causes of the bark-stripping behavior in Tataka. We also used a generalized linear model to evaluate factors that may affect the probability of a tree having its bark stripped. Both our observations and the model predictions showed that sambar has a strong preference for bark of Pinus armandii, Photinia niitakayamensis, and Salix fulvopubeseens and for trees with diameter at breast height around 14 cm. Bark stripping mainly occurred between July and October when major forage was most abundant. However, sambar's need for bark surged in May when sambar abundance was moderate and decreased in October when sambar abundance was high. The seasonality of bark stripping was synchronized with the peak periods of antler development, fawn nursing, and spread of gastrointestinal parasites, suggesting that sambar strips bark to ingest minerals for their physiological needs and/or to acquire plant secondary metabolites to repel gastrointestinal parasites. Sambar abundance alone was not sufficient to predict the overall intensity of bark stripping. Rather, the product of sambar abundance and the necessity index (average wound size) were strongly correlated with the overall bark-stripping intensity. Therefore, controlling sambar abundance is essential but it alone may not be the optimal strategy for controlling bark stripping. A combination of population control and relaxing of sambar's parasite loading and/or physiological needs for minerals is an important strategy to control the overall bark stripping. Future research could use the necessity index to investigate the synchronicity of the bark-stripping behavior, deer's physiological state, environmental factors and phenology to better understand the cause of this behavior.

Calcitriol and enamel matrix derivative differentially regulated cemento-induction and mineralization in human periodontal ligament-derived cells.

BACKGROUND: Alveolar bone and cementum share many biological and developmental similarities. The mineralizing effect of calcitriol has been previously reported. Yet, its cemento-inductivity has not been confirmed. This study evaluated the potential cemento-inductivity effect of calcitriol and enamel matrix derivative (EMD) on human periodontal ligament-derived cells (hPDLCs). METHODS: The hPDLCs obtained from extracted third molars or premolars were cultured with calcitriol, or EMD. Cementogenic gene expression was examined using real-time quantitative reverse transcription polymerase chain reaction. Expression analysis also included cementoblast-specific markers, cementum protein 1 (CEMP1), cementum attachment protein (CAP), and recently reported cementoblast-enriched genes, secreted frizzled related protein 1 (SFRP1), and Dickkopf-related protein 1 (DKK1). Mineralization capacities were evaluated by alkaline phosphatase (ALP) activity, Alizarin Red, and Von Kossa staining followed by scanning electron microscope imaging and element mapping. RESULTS: Among tested conditions, 10 nM calcitriol enhanced most cementogenic gene expression, transforming growth factor-ß1, bone morphogenetic proteins (BMP-2 and BMP-4), core-binding factor subunit alpha-1/Runt-related transcription factor 2, Type I collagen, ALP, bone sialoprotein, osteopontin), osteocalcin, CEMP1, and CAP, and Wnt signaling negative modulators, SFRP1 and DKK1, along with highest ALP activity and mineralization formation in hPDLCs. However, only moderate CEMP1 protein was observed. In contrast, EMD stimulated stronger CEMP1 and CAP protein, but presented weaker mineralization capacity, hinting at the possibility that strong stimulation of mineralization might dominate cemetogenic specific factors and vice versa. CONCLUSIONS: Calcitriol demonstrated not only great osteoinductivity, but also the potential to induce cementogenic gene expression by initiating hPDLC differentiation and promoting mineralization. Compared with calcitriol, EMD promoted cemento-inductivity in hPDLCs at a later time point via highly expressed CEMP1 and CAP protein, but with less mineralization. Thus, calcitriol and EMD could provide differential enhancement of cemento-induction and mineralization, likely acting at various differentiation stages.

Gag-Pol Transframe Domain p6* Is Essential for HIV-1 Protease-Mediated Virus Maturation.

HIV-1 protease (PR) is encoded by pol, which is initially translated as a Pr160gag-pol polyprotein by a ribosomal frameshift event. Within Gag-Pol, truncated p6gag is replaced by a transframe domain (referred to as p6* or p6pol) located directly upstream of PR. p6* has been proposed as playing a role in modulating PR activation. Overlapping reading frames between p6* and p6gag present a challenge to researchers using genetic approaches to studying p6* biological functions. To determine the role of p6* in PR activation without affecting the gag reading frame, we constructed a series of Gag/Gag-Pol expression vectors by duplicating PR with or without p6* between PR pairs, and observed that PR duplication eliminated virus production due to significant Gag cleavage enhancement. This effect was mitigated when p6* was placed between the two PRs. Further, Gag cleavage enhancement was markedly reduced when either one of the two PRs was mutationally inactivated. Additional reduction in Gag cleavage efficiency was noted following the removal of p6* from between the two PRs. The insertion of a NC domain (wild-type or mutant) directly upstream of PR or p6*PR did not significantly improve Gag processing efficiency. With the exception of those containing p6* directly upstream of an active PR, all constructs were either noninfectious or weakly infectious. Our results suggest that (a) p6* is essential for triggering PR activation, (b) p6* has a role in preventing premature virus processing, and

Association of vitamin D3 with alveolar bone regeneration in dogs.

Designed sockets prepared on the mandibles of nine Beagle dogs were divided into three groups: Calcitriol +Alloplast, Alloplast and Empty. Five of the nine dogs received Vit.D3 and calcium supplement (Vit.D/Ca group), while the other four dogs without supplements were assigned to Non-Vit.D/Ca group. After 4 weeks, the extent of vertical ridge resorption (VRR), bone density (density), new bone formation (NBF) and implant stability quotient (ISQ) were measured. Following systemic Vit.D/Ca administration, the Empty subgroup showed significant differences from the Calcitriol + Alloplast subgroup on variants NBF/Density/VRR and the Alloplast subgroup on items NBF/Density/ISQ/VRR. Alternatively, the Calcitriol + Alloplast subgroup revealed higher values of NBF/Density/ISQ (P < 0.001) and a lower VRR value (P = 0.001) than the Alloplast subgroup. Although there were no significant differences in NBF (P = 0.349), density (P = 0.796), ISQ (P = 0.577) and VRR (0.979) comparisons on alloplast treatment between the Vit.D/Ca and Non-Vit.D/Ca groups, local application with Calcitriol + Alloplast demonstrated better NBF/Density/ISQ (P = 0.02 to <0.001) effects than which of Alloplast subgroups. Consequently, the results showed that both systemic and local vitamin D3 treatment might accelerate bone regeneration in dogs. Within the using dose, systemic vitamin D3 treatment displayed a superior stimulating effect than local vitamin D3 application did.

The potential effects of cholecalciferol on bone regeneration in dogs.

OBJECTIVES: The aim of this investigation was to evaluate the potential effects of the systemically delivered combination of calcium supplementation and cholecalciferol and of the locally applied biphasic calcium alloplast on the surgically produced alveolar sockets at the early healing stage in a dog model. MATERIALS AND METHODS: The mandibular pre-molars of nine Beagle dogs were extracted first. Three months later, four standardized sockets with a 4 mm in diameter and 6 mm deep cylinder were created bilaterally at healed extraction sites. The sockets on one side were grafted with biphasic calcium phosphate alloplast, whereas the defects on the other side were left un-grafted. The dogs were then randomly divided into two groups; five dogs received oral calcium and cholecalciferol combination (Vit.D/Ca) and were assigned to the test group (Vit.D/Ca Group). The other four dogs without Vit.D/Ca supplement were distributed to the control group (Non-Vit.D/Ca Group). The bone density (Density) and the implant stability quotient (ISQ) at prepared sites were measured 4 weeks later. The drawn bone cores were examined by a histomorphometric analysis for measurement of new bone formation (NBF). The amount of vertical ridge resorption (VRR) was evaluated. RESULTS: The Vit.D/Ca-treated subjects revealed significantly more NBF (P < 0.05), higher bone density (P < 0.05) and significantly less vertical ridge reduction (P < 0.05) in the healing sockets than those without Vit.D/Ca treatment. The non-grafted sockets demonstrated significantly more NBF (P < 0.05), higher bone density (P < 0.05), better ISQ value (P < 0.05) and more vertical ridge reduction (P < 0.05) than those in the grafted sockets. There was no significant difference between the serum data determined before and 4 weeks after experiment in Vit.D/Ca Group or Non-Vit.D/Ca Group. However, the changed value (post-op vs. pre-op) between the two groups was significant in the serum level of phosphate and parathyroid hormone (P = 0.05). CONCLUSION: The results of the present study indicated that the examined calcium phosphate alloplast may perform a function in alveolar ridge preservation while reducing the potential of NBF potential in the healing extraction socket. Also, the combination of calcium supplementation and cholecalciferol may have systemic effects on accelerating bone regeneration.