Turnaround time and barriers to treatment of newly diagnosed cancer in Uganda: a mixed-methods longitudinal study

IntroductionCancer represents a growing public health concern. Late-stage at diagnosis, limited access to effective treatment, and loss to follow-up are responsible for dismal outcomes.ObjectiveTo describe care pathways, turnaround times, and identify barriers to timely initiation of cancer treatmentMethodsUsing a sequential mixed-methods design involving focus group discussions, we followed up 50 participants between January, and June 2018. We computed the median observed turnaround time to treatment (TTT) at each care step and reported delay as deviations from the proposed ideal turnaround times.ResultsThe ideal TTT with either chemotherapy, or radiotherapy, or surgery was 8, 14, and 21 days respectively. At a median follow-up time of 35.5 days (IQR 17–66), only 29 of the 50 study participants had completed all steps between registration and initiation of treatment, and the observed median TTT was 16 days (9 – 22 days) for chemotherapy, and 30 days (17 – 49 days) for radiotherapy, reflecting a significant delay (p-value = 0.017). Reported barriers were; shortage of specialists, patients required visits to outside facilities for staging investigations, prohibitive costs, poor navigation system and time wastage.ConclusionsWhen compared to the recommended ideal turnaround time, there was significant institutional delay in access to chemotherapy and radiotherapy attributed to multiple external and internal healthcare system barriers.     

Myelofibrosis secondary to hyperparathyroidism.

We report on a young female who had presented with fatigue, bilateral knee pain and gait disturbance. Primary hyperparathyroidism was diagnosed together with splenomegaly and anemia. Bone marrow biopsy revealed myelofibrosis. A parathyroid adenoma was excised during surgical intervention. As early as three months after the operation, hematologic parameters improved along with bone markers without any other intervention. The control bone marrow biopsy demonstrated well marked regression in marrow fibrosis. Her spleen has also gradually decreased in size. These findings indicate that her myelofibrosis was the result of primary hyperparathyroidism. Anemia associated with primary hyperparathyroidism may be due to bone marrow fibrosis.     

单克隆抗体BDI-I导向的阿霉素白蛋白毫微球对人膀胱癌细胞的特异杀伤活性

用化学偶联法将抗人膀胱癌单克隆抗体分子偶联到阿霉素白蛋白毫微球上,构建了一个有靶向杀伤性的免疫毫微球,即:阿霉素白蛋白载单克隆抗体毫微球(ADR-NP-Ab)。改变阿霉素毫微球和单克隆抗体的反应分子比,确定了制备该免疫毫微球的最佳条件。经免疫荧光检测及显微照像分析证明,免疫毫微球可有效地和人膀胱癌细胞结合。体外杀伤试验表明,此免疫毫微球对靶细胞EJ有高度特异杀伤活性,而对无关的人直肠癌Lovo细胞则无明显作用。     

Bacterial meningitis in infants: sonographic findings

A retrospective study was performed on 78 patients (newborn to 2 years old) with clinically proved bacterial meningitis. Sonograms were obtained during the acute illness and medical records were reviewed. The spectrum of sonographic features of meningitis included normal scans (30 patients), ventriculomegaly (11 patients), echogenic sulci (31 patients), extra-axial fluid collections (26 patients), abnormal parenchymal echogenicity (9 patients), evidence of ventriculitis (5 patients), and brain abscess (1 patient). In 46 patients, correlation between the sonographic findings and neurologic outcome on clinical follow-up (6 months to 4 years) was made. Findings of abnormal parenchymal echogenicity and/or moderate-to-marked ventriculomegaly were associated with significant neurologic sequelae; however, echogenic sulci and small extra-axial fluid collections did not appear to have any prognostic significance. Twenty-nine of the 78 patients had sonography without clinical indication of complications of meningitis, and in no patient was a significant abnormality found. Our study suggests that sonography is indicated only when there is clinical suspicion of complications.     

The role of oncogenes, tumour suppressor genes and growth factors in oral squamous cell carcinoma: a case of apoptosis versus proliferation

Mutation, deactivation and disregulated expression of oncogenes and tumour-suppressor genes may be involved in the pathogenesis of oral squamous cell carcinoma (SCC). Deactivation of the p53 tumour-suppressor gene allows cell proliferation and blocks apoptosis of malignant oral keratinocytes. Mutation in the ras oncog-ene results in persistent mitogenic signalling. Upregul-ated c-Myc expression, in the presence of growth factors, provides an additional proliferative signal. Loss of retino-blastoma tumour-suppressor gene (Rb) function may contribute to oral keratinocyte hyperproliferation and recent evidence suggests that simultaneous deactivation of both p53 and Rb is required for tumourigenesis. Enhanced Bcl-2 and reduced Fas expression inhibit tumour cell apoptosis and may convey resistance to cyto-toxic drugs and T cell-mediated cytotoxicity, respectively. Exogenous mutagens such as tobacco, alcohol and viral oncogenes may cause altered expression of oncogenes and tumour-suppressor genes in some cases of oral SCC. The impact of these mechanisms on future therapies for oral SCC is highlighted.