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91.
In the face of the current changes in land use and climate as well as habitat destruction, it is important to study herbaceous vegetation as an indicator of changes occurring in savanna ecosystems. We investigated the effects of climate, land use and habitat, both alone and in combination, on the diversity and occurrence of West African savanna herbaceous plant communities. Floristic data and environmental variables were sampled in Burkina Faso and subjected to ordination and indicator species analysis to explore the variation in nine vegetation types. Regression analyses showed that climate, land use, humidity gradient, soil fraction and vegetation structure discriminate herbaceous plant communities. Climate, habitat and their interaction had the greatest effect on the occurrence of these communities. Changes in species richness of the studied communities were mainly due to climate, land use and their interaction, which were more important for increasing rather than decreasing diversity. In all cases, climate conditions remained the most important environmental factor driving vegetation variation in West African savannas. Beside this, the effects of habitat degradation in interaction with land use and climatic conditions indicate land use to be a threat for the diversity of the herbaceous vegetation.  相似文献   
92.
The infection rate of Helicobacter pylori in children from < 1 to 17 years old was investigated. Three techniques, namely culture, CLO test, and PCR, were employed to check the presence or absence of the organism in the antrum of the stomach. Several PCR positives without viable cultures were observed in babies of less than one year old. On the other hand, only two viable cultures were obtained from toddlers of less than two years old. The percentage of positive cultures steadily increased from 8% (3 of 42 cases) in the 0-4 years old age group to 32% (32 of 99 cases) in the 13-17 years old age group. A steady increase also was observed in the result of the CLO test. In PCR, the percentage of positives was greatly higher than that seen with the culture or CLO test. The rate of PCR positives also showed an increase with age but of a much slower rate. The overall infection rate in 295 children was 22% (64 of 295 cases) positive with culture and 76% (225 of 295 cases) with PCR, in contrast to 85% (40 of 49 cases) and 92% (43 of 47 cases), respectively, in adults. The urease activity of the H. pylori derived from children was much lower than that derived from adults (P < 0.001). Taken together, these results suggest that a child might be repeatedly infected and some infecting strains eventually might obtain a steady infection, perhaps by a strain of higher virulence such as higher urease activity. The base variations in the nucleotide sequences did not correlate to the varied urease activities or to the age of the child. The sequences, however, indicated that there were two types of strains. The strains in Taiwan appeared to be derived from the French type strain and not the English type strain. The amino acid sequences of the ureA and the phylogenetic relationship of the 29 strains indicated that the strains in Taiwan are rapidly evolving into a unique clone.  相似文献   
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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by the death of motor neurons. A fundamental pathogenesis of ALS is the prolonged cell stress in neurons, which is caused by either accumulation of protein aggregates or reactive oxygen species. However, the mechanistic link between stress sensing and cell death is unsettled. Here, we identify that miR‐183‐5p, a neuron‐enriched miRNA, couples stress sensing and cell death programming in ALS. miR‐183‐5p is immediately induced by hydrogen peroxide, tunicamycin or TNF‐α in neurons. The overexpression of miR‐183‐5p increases neuron survival under stress conditions, whereas its knockdown causes neuron death. miR‐183‐5p coordinates apoptosis and necroptosis pathways by directly targeting PDCD4 and RIPK3, and thus protects neurons against cell death under stress conditions. The consistent reduction of miR‐183‐5p in ALS patients and mouse models enhances the notion that miR‐183‐5p is a central regulator of motor neuron survival under stress conditions. Our study supplements current understanding of the mechanistic link between cell stress and death/survival, and provides novel targets for clinical interventions of ALS.  相似文献   
95.
Hydroxychloroquine, used to treat malaria and some autoimmune disorders, potently inhibits viral infection of SARS coronavirus (SARS-CoV-1) and SARS-CoV-2 in cell-culture studies. However, human clinical trials of hydroxychloroquine failed to establish its usefulness as treatment for COVID-19. This compound is known to interfere with endosomal acidification necessary to the proteolytic activity of cathepsins. Following receptor binding and endocytosis, cathepsin L can cleave the SARS-CoV-1 and SARS-CoV-2 spike (S) proteins, thereby activating membrane fusion for cell entry. The plasma membrane-associated protease TMPRSS2 can similarly cleave these S proteins and activate viral entry at the cell surface. Here we show that the SARS-CoV-2 entry process is more dependent than that of SARS-CoV-1 on TMPRSS2 expression. This difference can be reversed when the furin-cleavage site of the SARS-CoV-2 S protein is ablated or when it is introduced into the SARS-CoV-1 S protein. We also show that hydroxychloroquine efficiently blocks viral entry mediated by cathepsin L, but not by TMPRSS2, and that a combination of hydroxychloroquine and a clinically-tested TMPRSS2 inhibitor prevents SARS-CoV-2 infection more potently than either drug alone. These studies identify functional differences between SARS-CoV-1 and -2 entry processes, and provide a mechanistic explanation for the limited in vivo utility of hydroxychloroquine as a treatment for COVID-19.  相似文献   
96.
Streptococcus mutans (S. mutans) uses a quorum sensing (QS) signaling system, which is dependent on competence stimulating peptide (CSP), to regulate diverse physiological activities including bacteriocin production, genetic transformation, and biofilm formation. However, the mechanism of the QS system-induced biofilm formation remains unclear. Here, we demonstrated that the late-stage biofilm formation was increased by the addition of exogenous CSP in S. mutans. The numbers of dead cells in biofilms formed in presence of CSP was 64.5% higher than that without CSP after 12 h (p < 0.05) and 76.3% higher after 24 h (p < 0.05), the numbers of live cells in biofilms formed in presence of CSP were 89.3% higher than that without CSP after 24 h (p < 0.01). The expression of QS-associated genes was increased 3.4-5.3-fold by CSP in biofilms. Our results revealed that cell viability of S. mutans grown in biofilms is affected by the CSP-dependent QS system.  相似文献   
97.
Li D  Li H  Ou C  Lu Y  Sun Y  Yang B  Qin Z  Zhou Z  Li S  Jin L 《PloS one》2008,3(5):e2168

Background

At the southern entrance to East Asia, early population migration has affected most of the Y-chromosome variations of East Asians.

Methodology/Principal Findings

To assess the isolated genetic structure of Hainan Island and the original genetic structure at the southern entrance, we studied the Y chromosome diversity of 405 Hainan Island aborigines from all the six populations, who have little influence of the recent mainland population relocations and admixtures. Here we report that haplogroups O1a* and O2a* are dominant among Hainan aborigines. In addition, the frequency of the mainland dominant haplogroup O3 is quite low among these aborigines, indicating that they have lived rather isolated. Clustering analyses suggests that the Hainan aborigines have been segregated since about 20 thousand years ago, after two dominant haplogroups entered East Asia (31 to 36 thousand years ago).

Conclusions/Significance

Our results suggest that Hainan aborigines have been isolated at the entrance to East Asia for about 20 thousand years, whose distinctive genetic characteristics could be used as important controls in many population genetic studies.  相似文献   
98.
Although p53 is frequently mutated in human cancers, about 80% of human melanomas retain wild-type p53. Here we report that PHGDH, the key metabolic enzyme that catalyzes the rate-limiting step of the serine biosynthesis pathway, is a target of p53 in human melanoma cells. p53 suppresses PHGDH expression and inhibits de novo serine biosynthesis. Notably, upon serine starvation, p53-mediated cell death is enhanced dramatically in response to Nutlin-3 treatment. Moreover, PHGDH has been found recently to be amplified frequently in human melanomas. We found that PHGDH overexpression significantly suppresses the apoptotic response, whereas RNAi-mediated knockdown of endogenous PHGDH promotes apoptosis under the same treatment. These results demonstrate an important role of p53 in regulating the serine biosynthesis pathway through suppressing PHGDH expression and reveal serine deprivation as a novel approach to sensitize p53-mediated apoptotic responses in human melanoma cells.  相似文献   
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