1
The sd-tg model thus provides direct evidence for secondary rearrangement at VH-D-JH.
2
In contrast, bone turnover and bone mass remained unchanged in tg arthritic mice.
3
Similar pathology was observed in the brains of GFAP-gp120 tg mice.
4
LEA-tg ICCs displayed the same potential to normalize glucose homeostasis as wild-type ICCs after transplantation.
5
Immunostaining for complement proteins was weak in tg mice but very strong in AD deposits.
6
Both tg and WT mice developed acute arthritis in response to the administration of collagen antibodies.
7
Despite the faster tooth movement, c-Fos tg and WT mice displayed the same amount of root resorption.
8
Osteoclast activity and bone resorption marker were increased in WT males following CMS, features absent in HSD2OB-tg males.
9
The abundant amyloid deposits in tg mice were in a consolidated state as revealed by strong Congo red birefringence.
10
Our results suggest that increased levels of tau negatively influence secretagogin expression in the hippocampus of tau tg mice.
11
Furthermore, both tibial cortical area and area fraction were reduced in stressed WT but not in stressed HSD2OB-tg male mice.
12
Severe morphological damage, including lipofuscin accumulation and mitochondria abnormalities, were found in aged tg-APP-SOD but not in the other mice.
13
These findings are consistent with a reduction in GABAA receptor-mediated synaptic inhibition during bursting in the tg CA3 hippocampal network.
14
Therapeutic strategies for the treatment of AD based on tg mouse models that overexpress Abeta may be limited in their application.
15
The tg is a typical null mutation due to the insertion of a transgene into the promoter region of MITF gene.
16
Thus, a combined elevation of the two chromosome 21 genes in tg-APP-SOD mice induced age-dependent alterations in morphological and behavioural functions.
