scholarly journals In vitro myotrophic effect of serum kappa chain immunoglobulins from a patient with kappa light chain myeloma and muscular hypertrophy.

1986 ◽  
Vol 78 (4) ◽  
pp. 922-927 ◽  
Author(s):  
C Delaporte ◽  
B Varet ◽  
M Fardeau ◽  
D Nochy ◽  
A Ract
1983 ◽  
Vol 211 (1) ◽  
pp. 173-180 ◽  
Author(s):  
J Y Chang ◽  
H Herbst ◽  
R Aebersold ◽  
D G Braun

The first complete sequence of the variable region of a kappa-light chain (V kappa) from a mouse anti-(streptococcal group A polysaccharide) antibody (immunoglobulin 7S34.1) is reported. Immunoglobulin 7S34.1 was isolated from the ascitic fluid of hybridoma 7S34.1 previously cloned in vitro. A newly developed technique for the isolation of peptides by using pre-column formation of peptide derivatives with dimethylaminoazobenzene isothiocyanate also served to complete the sequence. The sequence of the variable region of the kappa-light chain of immunoglobulin 7S34.1 defines a new mouse V kappa isotype (V kappa 27) and is the first mouse immunoglobulin light-chain variable region to be shown to have an extra cysteine residue at position 48.


2020 ◽  
Vol 6 (2) ◽  
pp. 81-90
Author(s):  
Adryan Fristiohady ◽  
Mini Bekti Ningsih ◽  
Fadhliyah Malik

Kanker payudara merupakan kanker yang paling banyak menyerang perempuan. Diperkirakan jumlah kasus tidak kurang dari 1.050.346 per tahun. Berdasarkan estimasi International Agency for Research on Cancer, diperkirakan pada tahun 2020 akan ada 1,15 juta kasus kanker payudara dengan 411.000 kematian. Kanker payudara adalah penyakit yang ditandai adanya jaringan payudara yang tumbuh secara invasif sehingga dapat menyebabkan kematian. Aktivasi NF-B yang berlebihan dan dideregulasi menyebabkan inflamasi yang tidak terkontrol. Respon inflamasi sistemik dan teregulasi adalah bagian dari pertahanan tubuh terhadap cedera, infeksi dan penyakit. Sehingga menekan jalur aktivasi NF-κB  dan menekan NF-κB adalah strategi yang menarik untuk pengembangan  molekul anti-inflamasi. Penulisan Review jurnal ini menggunakan studi pustaka tentang peranNF-κB terhadap kanker payudara dengan melihat aktivitas proliferasi dan apoptosis secarain vivo dan in vitro.


2019 ◽  
Vol 18 (2) ◽  
pp. 176-182
Author(s):  
Chen Weiyan ◽  
Deng Wujian ◽  
Chen Songwei

Acute lung injury is a clinical syndrome consisting of a wide range of acute hypoxemic respiratory failure disorders. Sepsis is a serious complication caused by an excessive immune response to pathogen-induced infections, which has become a major predisposing factor for acute lung injury. Taxifolin is a natural flavonoid that shows diverse therapeutic benefits in inflammation- and oxidative stress-related diseases. In this study, we investigated the role of taxifolin in a mouse model of cecal ligation and puncture-induced sepsis. Cecal ligation and puncture-operated mice presented damaged alveolar structures, thickened alveolar walls, edematous septa, and hemorrhage compared to sham-treated controls. Cecal ligation and puncture mice also showed increased wet-to-dry (W/D) lung weight ratio and elevated total protein concentration and lactate dehydrogenase level in bronchoalveolar lavage fluid. Taxifolin treatment protected animals against sepsis-induced pulmonary damage and edema. Septic mice presented compromised antioxidant capacity, whereas the administration of taxifolin prior to cecal ligation and puncture surgery decreased malondialdehyde concentration and enhanced the levels of reduced glutathione and superoxide dismutase in mice with sepsis-induced acute lung injury. Moreover, cecal ligation and puncture-operated mice showed markedly higher levels of proinflammatory cytokines relative to sham-operated group, while taxifolin treatment effectively mitigated sepsis-induced inflammation in mouse lungs. Further investigation revealed that taxifolin suppressed the activation of the nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway in cecal ligation and puncture-challenged mice by regulating the phosphorylation of p65 and IκBα. In conclusion, our study showed that taxifolin alleviated sepsis-induced acute lung injury via the inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells signaling pathway, suggesting the therapeutic potential of taxifolin in the treatment sepsis-induced acute lung injury.


1980 ◽  
Vol 255 (11) ◽  
pp. 5291-5295
Author(s):  
T. Kataoka ◽  
M. Ono ◽  
M. Kawakami ◽  
Y. Ikawa ◽  
M. Aida ◽  
...  

2020 ◽  
Vol 48 (12) ◽  
pp. 030006052097142
Author(s):  
Xiao-qing Yang ◽  
Sheng-you Yu ◽  
Li Yu ◽  
Lin Ge ◽  
Yao Zhang ◽  
...  

Objective To investigate the mechanism through which tacrolimus, often used to treat refractory nephropathy, protects against puromycin-induced podocyte injury. Methods An in vitro model of puromycin-induced podocyte injury was established by dividing podocytes into three groups: controls, puromycin only (PAN group), and puromycin plus tacrolimus (FK506 group). Podocyte morphology, number, apoptosis rate and microtubule associated protein 1 light chain 3 alpha ( LC3) expression were compared. Results Puromycin caused podocyte cell body shrinkage and loose intercellular connections, but podocyte morphology in the FK506 group was similar to controls. The apoptosis rate was lower in the FK506 group versus PAN group. The low level of LC3 mRNA observed in untreated podocytes was decreased by puromycin treatment; however, levels of LC3 mRNA were higher in the FK506 group versus PAN group. Although LC3-I and LC3-II protein levels were decreased by puromycin, levels in the FK506 group were higher than the PAN group. Fewer podocyte autophagosomes were observed in the control and FK506 groups versus the PAN group. Cytoplasmic LC3-related fluorescence intensity was stronger in control and FK506 podocytes versus the PAN group. Conclusions Tacrolimus inhibited puromycin-induced mouse podocyte damage by regulating LC3 expression and enhancing autophagy.


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