Interaction of testisin with maspin and its impact on invasion and cell death resistance of cervical cancer cells

AbstractPrevious studies have shown that testisin promotes malignant transformation in cancer cells. To define the mechanism of testisin-induced carcinogenesis, we performed yeast two-hybrid analysis and identified maspin, a tumor suppressor protein, as a testisin-interacting molecule. The direct interaction and cytoplasmic co-localization of testisin with maspin was confirmed by immunoprecipitation and confocal analysis, respectively. In cervical cancer cells, maspin modulated cell death and invasion; however, these effects were inhibited by testisin in parallel experiments. Of interest, the doxorubicin resistance was dramatically reduced by testisin knockdown (P=0.016). Moreover, testisin was found to be over-expressed in cervical cancer samples as compared to matched normal cervical tissues. Thus, we postulate that testisin may promote carcinogenesis by inhibiting tumor suppressor activity of maspin.Structured summaryMINT-7712215, MINT-7712176: Testisin (uniprotkb:Q9Y6M0) binds (MI:0407) to Maspin (uniprotkb:P36952) by pull down (MI:0096)MINT-7712188: Testisin (uniprotkb:Q9Y6M0) and Maspin (uniprotkb:P36952) colocalize (MI:0403) by fluorescence microscopy (MI:0416)MINT-7712115: Testisin (uniprotkb:Q9Y6M0) physically interacts (MI:0915) with Maspin (uniprotkb:P36952) by two-hybrid (MI:0018)MINT-7712162, MINT-7712128: Maspin (uniprotkb:P36952) physically interacts (MI:0915) with Testisin (uniprotkb:Q9Y6M0) by anti bait co-immunoprecipitation (MI:0006)MINT-7712147: Testisin (uniprotkb:Q9Y6M0) physically interacts (MI:0915) with Maspin (uniprotkb:P36952) by anti tag co-immunoprecipitation (MI:0007

Office management of lost intrauterine devices either with or without strings

AbstractObjectiveTo evaluate the efficacy of our method for retrieval of lost intrauterine devices (IUDs) either with or without strings in an office-based setting.MethodsA total of 38 women underwent retrieval of lost IUD. After preevaluation with ultrasonography and hysteroscopy, a Lin polyp grasper was used to remove the IUD under ultrasound monitoring without using a simultaneous hysteroscopy.ResultsOut of 38 women, 12 (31.6%) had IUD insertion for 10–19 years, whereas in another 12 women (31.6%), the duration was 20–40 years. Participants were divided into two groups: (1) premenopausal group (n = 21). The removed IUDs were 11 Chinese IUDs, seven FD-1 IUDs, one Yusei ring IUD, one Lippe loop IUD, and one Mirena IUD; and (2) postmenopausal group (n = 17). The removed IUDs were five soft type Ota ring IUDs, eight FD-1 IUDs, one Saf-T-Coil IUD, one KS wing IUD, and one Chinese IUD. A very hard type Ota ring IUD inserted for 40 years could not be removed. All of the other IUDs were removed uneventfully. Most of the patients could tolerate the procedure without the use of analgesia or anesthesia. No subsequent complication except bleeding for several days was encountered.ConclusionUsing our method, lost IUDs either with or without strings can be effectively and safely retrieved in the office-based setting without analgesia or anesthesia

Differential effect of corn oil-based low trans structured fat on the plasma and hepatic lipid profile in an atherogenic mouse model: comparison to hydrogenated trans fat

<p>Abstract</p> <p>Background</p> <p><it>Trans </it>fat are not desirable in many aspects on health maintenance. Low <it>trans </it>structured fats have been reported to be relatively more safe than <it>trans </it>fats.</p> <p>Methods</p> <p>We examined the effects of low <it>trans </it>structured fat from corn oil (LC), compared with high <it>trans </it>fat shortening, on cholesterol and fatty acid metabolism in apo E deficient mice which is an atherogenic animal model. The animals were fed a high <it>trans </it>fat (10% fat: commercial shortening (CS)) or a low <it>trans </it>fat (LC) diet for 12 weeks.</p> <p>Results</p> <p>LC decreased apo B and hepatic cholesterol and triglyceride concentration compared to the CS group but significantly increased plasma total cholesterol and triglyceride concentration and fecal lipids with a simultaneous increase in HDL-cholesterol level, apo A-I, and the ratio of HDL-cholesterol to total cholesterol (HTR). Reduction of hepatic lipid levels by inclusion of LC intake was observed alongside modulation of hepatic enzyme activities related to cholesterol esterification, fatty acid metabolism and fecal lipids level compared to the CS group. The differential effects of LC intake on the plasma and hepatic lipid profile seemed to be partly due to the fatty acid composition of LC which contains higher MUFA, PUFA and SFA content as well as lower content of <it>trans </it>fatty acids compared to CS.</p> <p>Conclusions</p> <p>We suggest that LC may exert a dual effect on plasma and hepatic lipid metabolism in an atherogenic animal model. Accordingly, LC, supplemented at 10% in diet, had an anti-atherogenic effect on these <it>apo E</it>^{<it>-/- </it>}mice, and increased fecal lipids, decreased hepatic steatosis, but elevated plasma lipids. Further studies are needed to verify the exact mode of action regarding the complex physiological changes and alteration in lipid metabolism caused by LC.</p