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This was a retrospective chart review in Western Australia, Australia.To describe the diagnosis, management, and treatment outcomes of ocular TB in Western Australia (WA).This was a retrospective review of ocular TB cases in WA from 2007 to 2018 with a minimum 2-year follow-up upon completion of anti-TB therapy (ATT).A total of 44 patients were referred to WA TB clinic. Ten were excluded from the analysis of treatment response; 34 met the inclusion criteria, of whom 97.1% were born overseas. No patients had symptomatic extraocular TB. Chest X-ray showed prior pulmonary TB in 11.7% of patients (n = 4). All patients were treated with three or four ATT drugs. The most common ocular TB manifestation was retinal vasculitis (23.5%). Full resolution of ocular inflammation following ATT occurred in 66.7% (n = 22), and reduced ocular inflammation requiring only topical steroid treatment was seen in 21.2% (n = 7). Treatment failure occurred in 12.1% (n = 4). Side effects were reported in 45.6% of patients, with gastrointestinal symptoms most common (27.2%).Our study is the first Australian study examining the management of ocular TB. Our study highlights the challenges in diagnosing TB ocular disease in a low-endemicity setting and the importance of the collaboration between uveitis and TB subspecialists..

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BACKGROUND: Oxytocin (OT) reduces rat duodenal tone and mouse intestinal transit; however, the underlying mechanisms are not totally understood. Consequently, this study was designed to investigate the influence of OT on spontaneous mechanical activity and neurally evoked responses, to characterize the mechanisms of the action, and to determine the distribution of the OT receptor (OTR) in rat proximal colonic muscle strips. METHODS: The organ bath technique with electrical field stimulation, western blotting, and immunofluorescence were used. KEY RESULTS: In rat proximal colon, exogenous OT induced a concentration-dependent reduction of the spontaneous mechanical activity without affecting the resting basal tone, which was abolished by atosiban, an OTR antagonist, by tetrodotoxin (TTX), a neural blocker or by Nω-propyl-l-arginine hydrochloride, an inhibitor of neuronal nitric oxide synthase (nNOS). The inhibitory effects of OT were not affected by atropine or the vasoactive intestinal peptide (VIP) receptor antagonist [Lys1, Pro2,5, Arg3,4, Tyr6]-VIP (VIPHyb). Proximal colon responses to electrical field stimulation were characterized by nonadrenergic, noncholinergic (NANC) relaxation, which was followed by an off-contraction. Oxytocin enhanced only NANC relaxation. Oxytocin stimulated spontaneous NO release from the longitudinal muscle myenteric plexus preparation of rat proximal colon. Western blot and immunohistochemistry experiments showing the presence of the OTR in proximal colon, and its co-localization with nNOS established that myenteric nitrergic neurons express OTR. CONCLUSIONS & INFERENCES: The activation of OTR located on nitrergic neurons may negatively modulate colonic spontaneous contraction and enhance electrically evoked NANC relaxation through excitation of NO release.

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OBJECTIVE: To evaluate the interference of hemoglobin variants J-Bangkok on glycated hemoglobin (HbA(1)c) detected by five measurement systems. METHODS: Seventy cases of blood samples were collected at Zhongshan Hospital of Sun Yat-sen University from July 2012 to January 2014, the blood samples were divided into the normal control group (40 cases) and Hb J-Bangkok variant group (30 cases), and the normal control group was divided into healthy control group (20 cases) and diabetic group (20 cases). HbA(1)c measurement systems were Primus Ultra2, Variant Ⅱ, Variant Ⅱ Turbo, Modular P and Leadman. Based on the standard of the American National Glycosylated Hemoglobin Standardization Program (NGSP), Primus Ultra2 was used as comparative system, and the other 4 systems were test systems. Comparative analysis and bias evaluation were conducted on the results from five detection systems in different groups, statistical analysis were used for evaluating the differences. The estimated average glucose (eAG) was calculated by HbA(1)c values and fasting plasma glucose (FPG) of Hb J-Bangkok variant group with the different detection systems. Deming regression analysis was used to determinate whether Hb J-Bangkok produced significant clinical effect on HbA(1)c results. HbA(1)c ± 10% and relative bias at 6% and 9% HbA1c were evaluation limits. RESULTS: The differences of the 95% confidence interval (95%CI) between the test systems and the comparative system in control group were within ±0.7% HbA(1)c, bias were less than 6%, there were no statistically significant difference (P>0.05). In Hb J-Bangkok group, the eAG calculated from HbA(1)c measured by using Primus Ultra2, Modular P and Leadman were (8.14±2.99), (8.10±3.06) and (8.23±3.00)mmol/L, which had no statistically significant difference compared with FPG ((8.21±3.12)mmol/L, t=0.996, 1.091, 1.479, all P>0.05), and the differences of 95%CI between the results measured by Modular P and the comparative system were all within ±0.7% HbA(1)c, bias were -4.3%-0.4% and -5.2%-4.9%, there were no statistically significant difference (P>0.05). At 6% and 9% HbA(1)c concentrations, the mean differences of the results from the three detection systems were less than the clinically acceptable range. These results showed that the systems of Primus Ultra2, Modular P and Leadman were not affected by Hb J-Bangkok. However, the eAG values calculated from HbA(1)c of Variant Ⅱ and Variant Ⅱ Turbo were (5.58±2.12) and(5.00±2.13)mmol/L, which showed statistically significant lower results compared with FPG level (t=12.29, 13.23 , all P<0.001). Compared with Primus Ultra2, the differences of 95%CI were outside of ± 0.7% HbA1c, bias were -31.9%--12.0% and -42.0%- -17.6% , greater than 6%, showed a negative bias.At 6% and 9% HbA(1)c concentrations, the mean differences of the results were all greater than the clinical acceptable range. These results indicated that Hb J-Bangkok had significantly clinical interference on Variant Ⅱ and Variant Ⅱ Turbo systems. CONCLUSION: Hb J-Bangkok has different interference on different HbA(1)c measurement systems, when performs the HbA(1)c test, clinical laboratory should pay attention to identify Hb variants, and select the appropriate methods to measure the HbA(1)c values in order to prevent the occurrence of interference by Hb variants.

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The mechanisms mediating the activation of cardiac gene expression during pressure overload are not fully understood. We examined whether angiotensin II-induced activation of ventricular gene expression is related to blood pressure and ventricular mass or requires other factors by infusing angiotensin II in sham-operated and adrenalectomized rats. In sham-operated rats, angiotensin II (33 microg/kg x h, sc) produced a significant increase in mean arterial pressure (measured by telemetry) within 3 h. Mean arterial pressure (up to 45 h) and the increase in left ventricular hypertrophy in adrenalectomized rats during angiotensin II infusion were similar to those in sham-operated rats. Angiotensin II produced 3.6-fold (P < 0.01) and 20.4-fold (P < 0.001) increases in ventricular atrial natriuretic peptide mRNA levels at 12 and 72 h, respectively. Angiotensin II infusion for 12 h also significantly increased the ventricular mRNA levels of B-type natriuretic peptide (5.2-fold) and adrenomedullin (1.4-fold). Adrenalectomy either abolished (atrial natriuretic peptide and adrenomedullin) or blunted (B-type natriuretic peptide) the early activation of ventricular gene expression by angiotensin II. The baseline synthesis of atrial natriuretic peptide, B-type natriuretic peptide, and adrenomedullin in the ventricle remained unchanged in adrenalectomized rats. In conclusion, our results indicate that factors derived from the adrenals are required for angiotensin II-induced early activation of cardiac gene expression.

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