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Poststreptococcal reactive arthritis （PSRA） refers to reactive arthritis after Group A streptococcal （GAS） infection that does not meet the diagnostic criteria for acute rheumatic fever （ARF）. It is rare in clinical practice and prone to misdiagnosis due to the lack of characteristic symptoms and signs in the early stage of PSRA. In this article， an adult male patient with PSRA was reported， showing recurrent swelling and pain on the back of the right foot and the medial malleolus. The onset process of the patient was suspected of gout. He received the treatment of reducing uric acid and relieving pain in a local hospital， which was ineffective. The patient was finally diagnosed with PSRA because of the history of pharyngitis and elevated levels of C-reactive protein and antistreptolysin O （ASO） through detection. He received long-term use of benzathine benzylpenicillin combined with anti-inflammatory and analgesic therapy. Subsequently， the condition was improved and no recurrence occurred during follow-up. The diagnosis and treatment of this case prompt that for patients with recurrent arthritis， the possibility of PSRA should be considered. Extensive attention should be paid to differential diagnosis and treatment between gout and reactive arthritis.

Under the background of "double carbon", building carbon emission reduction is urgent, and improving energy efficiency through short-term building heat load forecasting is an efficient means of building carbon emission reduction. Aiming at the characteristics of the decomposed short-term building heat load data, such as complex trend changes, significant seasonal changes, and randomness, a single-step short-term building heat load prediction method driven by the multi-component fusion LSTM Ridge Regression Ensemble Model (ST-LSTM-RR) is designed and implemented. First, the trend and seasonal components of the heat load are decomposed by the STL seasonal decomposition algorithm, which are fused into the original data to construct three diversified datasets; second, three basic models, namely, the trend LSTM, the seasonal LSTM, and the original LSTM, are trained; and then, the ridge regression model is trained to fuse the predicted values of the three basic models to obtain the final predicted values. Finally, the method of this paper is applied to the heat load prediction of eight groups in a large mountain hotel park, and the root mean square error (RMSE) and mean absolute error (MAE) are used as the evaluation indexes. The experimental results show that the average RMSE and average MAE of the prediction results of the proposed method in this paper are minimized on the eight groups. [ABSTRACT FROM AUTHOR]

Background: In previous studies, we confirmed that endogenous uric acid (UA) formation increases in the streptozotocin (STZ)-induced diabetic rats with renal injury. Yet changes of renal UA reabsorption and hepatic UA metabolism remain unclear in this model. Methods: STZ-induced diabetic rats and control rats were treated with benzbromarone (BZ), a glucose transporter 9 (GLUT9) inhibitor for 8 weeks. At baseline, 4 and 8 weeks after BZ treatment, blood samples were collected for fasting blood glucose (FBG), serum uric acid (SUA), serum creatinine (SCr), and blood urea nitrogen (BUN). Simultaneous urinary samples were tested and daily urinary amount of albumin (UAE), uric acid (UUA), creatinine (UCR), urea nitrogen (UUN) were calculated. Gene expressions of GLUT9, xanthine oxidase (XO), urate transporter 1 (URAT1) in the kidney and GLUT9, XO as well as uricase in the liver were detected by RT-PCR. Results: 1) Compared with normal rats, FBG, BUN, UUN, UAE and UUA were significantly increased, while SUA was significantly decreased in diabetic rats, while SCr and UCR levels were compared. Treatment with BZ did not change FBG in both rats. BZ significantly decreased SCr, BUN and UAE levels but increased SUA in diabetic rats. 2) In the kidney, expression of GLUT9 and XO was increased, while URAT1 was not altered in diabetic rats if compared with control rats. BZ treatment exerted no any effects on gene expression of GLUT9 and XO. 3) In the liver, gene expression of XO and uricase was compared between diabetic and normal rats, while GLUT9 was significantly upregulated in diabetic rats. BZ treatment remarkably inhibited GLUT9 expression but left XO and uricase unchanged in diabetic rats. Conclusions: 1) Inhibition of hepatic GLUT9 in STZ-induced diabetic rats increased SUA indicates that GLUT9 pathway for UA metabolism is critical in this model. 2) BZ treatment attenuates urinary albumin excretion in diabetes. Disclosure: C. Chen: None. J. Ran: None. R. Zhang: None. G. Chen: None. P. Zhu: None. J. Qiu: None. R. Tan: None. Y. Liu: None. [ABSTRACT FROM AUTHOR]