05). Multivariate Cox regression analysis revealed that XRCC1 or lymph node metastasis were independent risk factors of gastric cancer recurrence (P less then 0.05). Kaplan-Meier survival curve assay indicated that patients with low JWA or XRCC1 expression in gastric cancer had significantly shorter DFS than those with high-expressed proteins (P less then 0.05). JWA or XRCC1 may be effective markers to predict gastric cancer recurrence.Psoriasis is reportedly modulated by the Janus kinase (JAK)/signal transducer and activator of transcription (STAT) or vascular endothelial growth factor/p21-activated kinase 1 (VEGF/PAK1) pathways. However, no research has evaluated the expression of JAK/STAT and VEGF/PAK1 signaling pathway molecules in human psoriasis skin tissue concurrently. We investigated the expression of autocrine STAT1, STAT3, VEGF, suppressor of cytokine signaling-1 (SOCS1), SOCS3, and PAK1 in psoriatic tissues. Skin biopsies were retrospectively collected from 55 patients with psoriasis from the tissue biobank. Skin biopsies from 40 healthy volunteers undergoing plastic surgery were used as controls. check details Immunohistochemical staining revealed that STAT1, STAT3, SOCS1, SOCS3, VEGF, and PAK1 were present at significantly higher levels in the psoriasis samples compared to the control group. Similarly, the mRNA expression of these signaling molecules was also significantly upregulated in psoriatic skin. Additionally, some of the molecules in these two signaling pathways exhibited significant positive correlations. In summary, we present pilot evidence that JAK/STAT and VEGF/PAK1 signaling molecules are expressed in psoriasis, which may provide topical treatment targets for this disease.

As a chronic inflammatory skin disease of unknown etiology, vulvar leukoplakia mainly affects postmenopausal and peri-menopausal females. The main clinical manifestations of vulvar lichen sclerosus et atrophicus (VLSA) include itching, burning pain, and sexual dysfunction, which can lead to a decline in the quality of life. The existing treatment options include topical corticosteroid ointment, estrogen, and traditional Chinese medicine. However, their therapeutic effects on VLSA remain unsatisfactory. In the present study, we aimed to investigate the clinical efficacy and safety of photodynamic therapy (PDT) in combination with 5-aminoketovaleric acid (ALA) for the treatment of vulvar leukoplakia.

A total of 30 patients with VLSA who failed routine treatment were treated with ALA-PDT. The patients were irradiated at a power density of 60-90 mW/cm

with a red light at a wavelength of 635±15 nm for 20 min. Twenty percent of ALA water-in-oil emulsion was applied to the lesion and sealed with plastic film for 3 h. The treatment was repeated three times every 2 weeks. The objective and subjective symptoms and signs of vulvar lesions based on the horizontal visual analogue scale were recorded at 6 months after each treatment and the last treatment.

All patients completed three cycles of ALA-PDT and follow-up. The clinical symptoms of pruritus completely disappeared in 27 cases. Itching changed from severe to mild in three cases. The pathological changes of all subjects were improved. The main side effects of ALA-PDT were pain, erythema, and swelling. The side effects were temporary and tolerable. All patients reported their results as “satisfied” or “very satisfied”.

ALA-PDT was an effective and safe approach for the treatment of VLSA.

ALA-PDT was an effective and safe approach for the treatment of VLSA.

To quantify the expression of miR-195 and miR-497 in acute stroke and to evaluate their correlations with post-stroke cognitive impairment.

A total of 108 patients with acute stroke admitted to our hospital from January, 2019 to June, 2020 were enrolled as a patient group, and 76 healthy volunteers were recruited as a normal group. Levels of serum miR-195 and miR-497 in the two groups were quantified. Neurological and cognitive functions were tested by National Institutes of Health Stroke Scale (NIHSS) and Montreal Cognitive Assessment (MoCA), respectively. Diagnostic value of serum miR-195 and miR-497 in acute stroke was evaluated by receiver operating characteristic (ROC) curve, and independent risk factors were determined by multivariate logistic regression.

Levels of serum miR-195 and miR-497 increased in acute stroke. The area under the curve (AUC) of serum miR-195 in the diagnosis of acute stroke was 0.901, while that of serum miR-497 was 0.922. Levels of miR-195 and miR-497 were positively correlated with NIHSS score and negatively correlated with MoCA score. Logistic regression analysis demonstrated that family history of stroke, diabetes, hypertension, NIHSS score, MoCA score, miR-195, and miR-497 were independent risk factors for acute stroke.

Serum miR-195 and miR-497 are elevated in acute stroke and associated with the loss of neurologic and cognitive functions. They may be biomarkers for diagnosis and prognosis of acute stroke.

Serum miR-195 and miR-497 are elevated in acute stroke and associated with the loss of neurologic and cognitive functions. They may be biomarkers for diagnosis and prognosis of acute stroke.

Dysfunctions of microRNAs have been implicated in the progression of clear cell renal cell carcinoma (ccRCC). Here, we investigated the roles of miR-99b and miR-99b* in ccRCC development.

The expression levels of miR-99b and miR-99b* in tumor and tumor-adjacent tissues from ccRCC patients were quantified by quantitative Real-Time PCR (qRT-PCR). MicroRNA mimics and inhibitors were employed to evaluate the functions of miR-99b and miR-99b*. The effects of miR-99b on the proliferation and migration of ccRCC cells were analyzed by MTT and wound-healing assays, respectively. The effect of miR-99b on the expression of its target gene IGF1R and mTOR was determined by western blotting and qRT-PCR.

The abundances of miR-99b and miR-99b* were lower in ccRCC tissues than in the tumor-adjacent tissues from patients. Similarly, the expression of these two microRNAs was higher in the normal kidney HK-2 cells than in the ccRCC cell lines. Moreover, miR-99b and miR-99b* inhibited the proliferation and migration of ccRCC cells.