In this task, you are given an abstract of article. Your task is to generate title for this article. Preferred titles are under thirty words.

Example Input: [Purpose] The present study examined whether electro-acupuncture therapy reduces post-stroke depression (PSD) and whether motor function impairments interact with the effects of the therapy. [Subjects] Twenty-eight PSD patients were assessed and assigned to either a good or poor motor function group depending on their motor grade. [Methods] The Beck Depression Inventory (BDI), Hamilton Depression Rating Scale (HDRS) and Manual Muscle Test (MMT) were administered at the screening and initial phases of the study, and at the 4th, 8th, 12th and 16th week of the daily electro-acupuncture treatment. [Results] The electro-acupuncture treatment reduced PSD (as assessed by BDI and HDRS) of the patients. In particular, the depression of the good motor function group was significantly more reduced than that of the poor motor function group. The degree of motor function impairment did not change throughout the study in either group. [Conclusion] The results of the present study demonstrate that electro-acupuncture therapy can improve PSD, and that the treatment effect varies depending on the degree of motor function impairment.
Example Output: Effects of Electro-Acupuncture Therapy on Post-Stroke Depression in Patients with Different Degrees of Motor Function Impairments: a Pilot Study

Example Input: Excessive exposure to estradiol represents the main risk factor for endometrial cancer. The abnormally high estradiol levels in the endometrium of women with endometrial cancer are most likely due to overproduction by the tumour itself. Endometrial cancer cells express the genes encoding the steroidogenic enzymes involved in estradiol synthesis. Here we used RT-PCR and Western blot to show that the nuclear receptors SF1 and LRH1, two well-known regulators of steroidogenic gene expression in gonadal and adrenal cells, are also expressed in endometrial cancer cell lines. By transient transfections, we found that SF1 and LRH1, but not the related nuclear receptor NUR77, can activate the promoters of three human steroidogenic genes: STAR, HSD3B2, and CYP19A1 PII. Similarly, forskolin but not PMA, could activate all three promoters. In addition, we found that both SF1 and LRH1 can transcriptionally cooperate with the AP-1 family members c-JUN and c-FOS, known to be associated with enhanced proliferation of endometrial carcinoma cells, to further enhance activation of the STAR, HSD3B2, and CYP19A1 PII promoters. All together, our data provide novel insights into the mechanisms of steroidogenic gene expression in endometrial cancer cells and thus in the regulation of estradiol biosynthesis by tumour cells.
Example Output: The nuclear receptors SF1 and LRH1 are expressed in endometrial cancer cells and regulate steroidogenic gene transcription by cooperating with AP-1 factors.

Example Input: Consistent with previous reports, sphingosine at a high concentration (5 microM) was cardiotoxic as evidenced by increased infarct size in response to ischemia/reperfusion in an ex vivo rat heart. Sphingosine 1-phosphate (S1P) at 5 microM was cardioprotective. However, at a physiologic concentration (0.4 microM) sphingosine as well as S1P was effective in protecting the heart from ischemia/reperfusion injury both when perfused prior to 40 min of ischemia (preconditioning) or when added to reperfusion media following ischemia (postconditioning). Protection by sphingosine and S1P was evidenced with both pre- and post-conditioning by a >75% recovery of left ventricular developed pressure during reperfusion and a decrease in infarct size from 45% of the risk area to less than 8%. When VPC23019, an S1P(1and3)G-protein coupled receptor antagonist, was added to the preconditioning or postconditioning medium along with S1P, it completely blocked S1P-induced protection. However, VPC 23019 did not affect the ability of 0.4 microM sphingosine to either precondition or postcondition hearts. Studies of preconditioning revealed that inhibition of protein kinase C with GF109203X blocked preconditioning by S1P. However, GF109203X did not affect preconditioning by 0.4 microM sphingosine. Likewise, cotreatment with the PI3 kinase inhibitor wortmanin blocked preconditioning by S1P but not by sphingosine. By contrast, inhibition of protein kinase G with KT5823 had no effect on S1P preconditioning but completely eliminated preconditioning by sphingosine. Also, the protein kinase A inhibitory peptide 14-22 amide blocked preconditioning by sphingosine but not S1P. These data reveal for the first time that sphingosine is not toxic at physiologic concentrations but rather is a potent cardioprotectant that utilizes a completely different mechanism than S1P; one that is independent of G-protein coupled receptors and utilizes cyclic nucleotide-dependent pathways.
Example Output:
Sphingosine can pre- and post-condition heart and utilizes a different mechanism from sphingosine 1-phosphate.