Optic neuritis presented as the only manifestation of neurosyphilis.

Here, we report a case of syphilis presented with optic neuritis to consider neurosyphilis as one of the differential diagnoses of optic neuritis. A 25-year-old male attended at outpatient department of chittagong eye infirmary and training complex institute with a history of a sudden loss of vision in the left eye for 20 days. On eye examination, the patient had reduced visual acuity on the left eye (6/60), and the left pupil showed a relative afferent pupillary defect and swollen left optic disc. No other abnormalities were found in a routine blood test and magnetic resonance imaging of the brain. Intravenous corticosteroid was administered for 3 days followed by oral corticosteroid. His vision was gradually improving within a month and became 6/9 in the left eye, but after a month, the patient returned with the blurring of vision in the same eye for 3 days. An extensive serum biochemical and serological test and cerebrospinal fluid (CSF) analysis was done including syphilis serology and human immunodeficiency virus (HIV) serology. Venereal disease research laboratory (VDRL) test and Treponema pallidum hemagglutination assay (TPHA) were found positive with high titer (1:1280) and rapid plasma reagin (RPR) titer of 1:64 in blood. The CSF analysis showed leukocytosis, and VDRL and TPHA were also found positive with high RPR titer. The HIV serology test was negative. The patient was treated with injectable ceftriaxone 2 g intravenously for 14 days and also injectable corticosteroid. His vision was improved within this period. Unilateral optic neuritis due to syphilis without other ocular features is uncommon but should be considered if a patient presents with visual loss and optic disc swelling. Early diagnosis based on clinical suspicion and prompt management is important to prevent visual impairment and subsequent neurological complications.

Prediction of surfactant requirement in Indian preterm infants by lung ultrasound scores: a diagnostic accuracy study from a developing country.

The purpose of this study is to validate lung ultrasound score (LUS) for prediction of surfactant replacement therapy (SRT) in Indian infants of 27-336/7 weeks gestational age (GA). This prospective diagnostic accuracy study was conducted in a level 3 neonatal care unit in India. Consecutively born preterm infants with respiratory distress syndrome (RDS) were enrolled. Surfactant was administered if oxygen requirement exceeded > 30%. Baseline characteristics, respiratory parameters, and lung ultrasound images were recorded soon after admission and compared between surfactant and non-surfactant groups. Adjusted odds ratio (OR) and diagnostic accuracy of LUS were calculated for SRT. Among 78 infants with RDS included in the final analysis, 62 received surfactant (79.48%). Median time of performing lung ultrasound was 50 min of life in both groups. Median LUS in the anterior and posterior chest areas of either side as well as total LUS was significantly higher in the surfactant group. After adjusting for other confounders, LUS was found to be a significant predictor of SRT (adjusted OR (95%CI): 1.55 (1.15-2.087)). Diagnostic accuracy of LUS was determined by receiver operating characteristic (ROC) curve analysis (AUC (95% CI): 0.751 (0.64-0.842), p < 0.001). A cutoff score of ≥ 9 for LUS was considered optimal for SRT (sensitivity (95%CI): 70.97% (57.87-81.45), specificity (95%CI): 68.75% (41.48-87.87)). CONCLUSION: Lung ultrasound is a valid diagnostic tool for SRT in Indian setting with a cutoff score ≥ 9. TRIAL REGISTRATION: CTRI/2021/11/038269. WHAT IS KNOWN: • Surfactant requirement in preterm infants with RDS has been traditionally based on FiO2 criteria. • Lung ultrasound score can predict the need for surfactant although majority of the studies originated in developed countries. WHAT IS NEW: • Lung ultrasound is a valid tool for surfactant replacement therapy even in developing countries like India.

Carcinogen 7,12-dimethylbenz[a]anthracene-induced mammary tumorigenesis is accelerated in Smad3 heterozygous mice compared to Smad3 wild type mice.

Previous studies based on cell culture and xenograft animal models suggest that Smad3 has tumor suppressor function for breast cancer during early stages of tumorigenesis. In this report, we show that DMBA (7,12-dimethylbenz[a]anthracene), a chemical carcinogen, induces mammary tumor formation at a significantly higher frequency in the Smad3 heterozygous mice than in the Smad3 wild type mice. This is the first genetic evidence showing that Smad3 inhibits mammary tumor formation in a mouse model. Our findings support the notion that Smad3 has important tumor suppressor function for breast cancer.

Tumor associated release of interleukin-10 alters the prolactin receptor and down-regulates prolactin responsiveness of immature cortical thymocytes.

The soluble factors produced either by Ehrlich's ascites carcinoma (EAC) or thymic adherent cells (TAC) of tumor-bearing mice comprising of CD11b(+) and CD11c(+) antigen-presenting cells caused a sharp decrease in prolactin (PRL)-induced ConA-mediated effect on survival of PNA(+) thymocytes. Similar suppression of PRL-induced effect was observed when the cells were cocultured with TAC of EAC-bearing mice. Anti-IL-10 antibody could reverse the PRL inability to induce ConA-mediated effect on PNA(+) thymocyte survival, indicating the presence of IL-10 in EAC culture supernatant (EAC sup) and thymic microenvironment. IL-10 could block PRL-induced proliferation of PNA(+) thymocytes without affecting spontaneous apoptosis. IL-10 altered the expression of the long-form (LF) of PRL-R and reduced the PRL binding of the cells, suggesting down-regulation of the PRL effect on PNA(+) thymocyte by the cytokine. Induction of tumor, which was found to increase the IL-10 secretion by TAC, also modified the PRL-R (LF) to PRL-R (SF). Since PRL plays a role in survival, proliferation and differentiation of lymphoid progenitor cells, the tuning of PRL action by IL-10 may be a possible mechanism of depletion of immature cortical thymocytes and thymic atrophy in tumor-bearing mice.

Prolactin induced reversal of glucocorticoid mediated apoptosis of immature cortical thymocytes is abrogated by induction of tumor.

Glucocorticoid (GC) and prolactin (PRL) are the two neuroendocrines that regulate thymocyte differentiation and maintain the immune homeostasis during stress. We found that dexamethasone (Dex), a synthetic GC, induced apoptosis in normal immature cortical thymocytes which remained unaltered in the presence of Elrich's ascitic carcinoma (EAC). PRL protected the normal CD4+ CD8+ cortical thymocytes from Dex-induced apoptosis but failed to alter the effect of Dex in tumor-bearing mice. Dex-treated normal thymocytes became unresponsive to PRL in presence of tumor cell culture supernatant. Low binding affinity of the microsomal membranes of thymocytes to PRL and absence of the mRNA of a particular form of prolactin receptor (PRL-R) suggest the presence of a different PRL-R in CD4+ CD8+ thymocytes of EAC-bearing mice. The induction of tumor may alter the PRL-R that can be correlated with the failure of PRL in rescuing CD4+ CD8+ immature cortical thymocytes from GC induced death.