Many Canadian nursing programs endorse clinical placements abroad. We critically examined the hidden curriculum embedded in clinical placements seeking to provide a ‘global’ experience. Using purposeful sampling, we interviewed a total of 18 participants, including eight faculty, eight students and two placement coordinators. Data were analyzed using initial and focused coding, supported by NVivo. After generating themes from the coded data, we adapted Hafferty’s (1998) framework to further analyze the theme of the hidden curriculum. The findings illuminate how policies sustained international experience as a privileged endeavour, with restricted access based on grades. Placements incorporated little evaluation of benefits for local communities. Few resources were allocated to students for such placements, as many students paid for their placement. The institutional terms ‘international and global experience’ denoted interactions with cultural “Others”. We recommend that nursing programs attend to hidden practices that sustain clinical placements abroad as prestigious, commodified experiences.
Ablepharon macrostomia syndrome (AMS) is a rare congenital disorder. To our knowledge, only 20 cases have been reported to date, and all in patients from Western countries. We report a case of AMS in a Thai patient, who presented at age 3 months with severe ectropion of both upper and lower eyelids, alopecia totalis, no palpable clitoris, and hypoplasia of both labia minora and labia majora. Trio whole exome sequencing analysis was performed, which revealed a heterozygous missense c.223G>A (p.Glu75Lys) variation in TWIST2. To our knowledge, this is the first reported case of AMS in a patient from Thailand and the first reported case of AMS in Asia.
Epidermal growth factor receptor (EGFR) sequence variants in patients from Myanmar have not yet been reported.
To describe the molecular epidemiology of EGFR variants in patients from Myanmar with lung adenocarcinoma.
Histological diagnosis and categorization of biopsies collected from 66 patients (28–78 years) with lung cancer was conducted using a panel of antibodies including those to: TTF1, P40, synaptophysin, CK7, and napsin-A. Samples from patients with confirmed adenocarcinoma were tested for EGFR variants using a cobas EGFR Mutation Test kit and cobas z 480 System (Roche). We conducted a univariate analysis of categorical factors using a χ2 or Fisher exact test.
Histological types were adenocarcinoma (61%, 40/66), squamous cell carcinoma (24%, 16/66), neuroendocrine carcinoma (9%, 6/66), undifferentiated carcinoma (2%, 1/66), adenosquamous carcinoma (2%, 1/66), small cell anaplastic carcinoma (2%, 1/66), and pleomorphic sarcoma (2%, 1/66). EGFR variants were detected in 15 of 40 (38%) cases of adenocarcinoma. Among them, 6 patients (40%) had an exon 19 deletion, another 6 (40%) had exon 21 substitutions, 1 (7%) had exon 20 insertion S768I, and 2 (13%) had compound variations (1 of exon 21 L858R and exon 18 G719X, and 1 of exon 20 S768I and exon 18 G719X). Although limited by small sample size, no significant association was found between the variants and factors including family cancer history, age group, sex, ethnicity, or occupation. However, there was a strong significant association between never-smokers and EGFR variants (P = 0.008).
Knowledge of EGFR variants in patients from Myanmar is encouraging for their effective cancer treatment.
Nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) is a sophisticated transcription factor that is particularly important in the inflammatory response, but it regulates more than 400 individual and dependent genes for parts of the apoptotic, angiogenic, and proliferative, differentiative, and cell adhesion pathways. NF-κB function is directly inhibited by the binding of inhibitor of κB (IκB), and the imbalance between NF-κB and IκB has been linked to the development and progression of cancer and a variety of inflammatory disorders. These observations might broaden the horizon of current knowledge, particularly on the pathogenesis of inflammatory diseases considering the roles of NF-κB and IκB. In this context, we focus this narrative review on a comparative discussion of our findings with other literature regarding variations of NFKB1 and NFKB1A and their association with susceptibility to widespread inflammatory disorders (such as atherosclerosis, morbid obesity, Behçet syndrome, Graves disease, Hashimoto disease) and common cancers (such as gliomas).
In patients with phenylketonuria, the central nervous system is adversely affected by noncompliance with diet. The levels of phenylalanine and many different amino acids (AAs) in the plasma of patients with phenylketonuria can be measured simultaneously.
To measure the blood plasma levels of neurotransmitter AAs in a cohort of patients in Sanliurfa province, Turkey, with phenylketonuria for use as a support parameter for the follow-up of patients.
The phenylketonurics that we followed (n = 100) were divided into 2 groups according to their compliance with their dietary treatment. Plasma AA analysis results of phenylketonurics were compared with those of healthy children in a control group (n = 50).
In the diet incompliant group (n = 56), the mean levels of γ-aminobutyric acid (GABA; 0.96 ± 1.07 μmol/L) and glycine (305.1 ± 105.19 μmol/L) were significantly higher than those in the diet compliant group (n = 44; GABA P = 0.005, glycine P < 0.001) and in the control group (GABA and glycine P < 0.001), whereas the mean levels of glutamic acid (39.01 ± 22.94 μmol/L) and asparagine (39.3 ± 16.89 μmol/L) were lower (P < 0.001) in the diet incompliant group. A positive correlation was observed between the levels of phenylalanine and GABA and glycine. A negative relationship was found between the levels of phenylalanine and glutamic acid and asparagine.
A relationship exists between the levels of plasma phenylalanine in a cohort of phenylketonurics in Sanliurfa province, Turkey, and the levels of some excitatory and inhibitory AAs. Excitatory and inhibitory AA levels in plasma may be used as support parameters in the follow-up of patients with phenylketonuria.
Neonatal jaundice and elevated levels of liver enzymes are found in infants with breast milk jaundice (BMJ).
To determine the prevalence and duration of elevated serum levels of liver enzymes in Thai infants with BMJ.
We conducted a prospective study of Thai infants with BMJ, excluding those with pathological causes of jaundice. We measured the serum levels of total bilirubin (TB), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and γ-glutamyl transferase (GGT); followed infants with elevated levels; and estimated the time for levels to become normal using Kaplan–Meier analysis.
We included 42 infants (median age: 17.5 days) with BMJ, and elevated serum levels of at least 1 enzyme were found in 27 (64%) infants. We excluded 4 (10%) infants because they did not continue to be exclusively breastfed, 17 (40%) were lost to follow-up, and 21 (50%) completed the study. We found that 19 (45%) of the 42 infants had elevated GGT, 11 (26%) had elevated ALT, and 9 (21%) each had elevated AST and ALP levels. The median time for enzyme levels to normalize was 291 days (95% confidence interval [CI], 109.8 to 472.2) for ALT, 240 days (95% CI, 139.0 to 340.9) for AST, 184 days (95% CI, 4.4 to 363.6) for ALP, 120 days (95% CI, 74.6 to 164.5) for TB, and 63 days (95% CI, 61.44 to 64.6) for GGT. Infants were otherwise healthy during the follow-up.
The prevalence of elevated serum levels of liver enzymes in Thai infants was unexpectedly high, but the levels became normal spontaneously despite continued breastfeeding, which endorses a “watchful waiting” strategy in managing asymptomatic infants with BMJ.