METHOD: This retrospective cohort study evaluates the differences in surgical outcomes of THA vs HA in 85 patients with displaced intracapsular fractures, based on the time taken for patients to ambulate to walking frame/crutches and wheelchair post-operatively and the incidence of post-operative complications.
RESULTS: Patients who received HA were significantly older (p<0.0001, <0.05) and had poorer pre-operative ambulatory function (p=0.032, p<0.05) than those of the THA group. HA patients had a significantly faster recovery to walking frame/crutches (20.2 days) compared to THA patients (47.3 days) (Mann-Whitney U=447.500, n=46, p=0.043, <0.05 two-tailed). While no significant differences were found in deep vein thrombosis (DVT), infected prosthesis, or dislocation incidence, hospital-acquired pneumonia (HAP) was more prevalent in THA patients (p=0.044, <0.05). Time to the walking frame had a significant effect on DVT/PE (p<0.001,
METHODS: The cross-sectional study was performed during the third week of June among first to final year medical and dental students. As the country was in lockdown, a structured online questionnaire was used. The responses obtained were entered into IBM SPSS Statistics for Windows and the normality of the data checked using one-sample Kolmogorov Smirnov test. The demographic parameters were tabulated, and total score compared among different subgroups of participants. The frequency of different measures mentioned by respondents were also noted.
RESULTS: More than half of the participants were females (59.6%). Nearly half 282 (49.8%) belonged to age group 21-23 years. The majority 415 (73.5%) were undergraduate medical and 150 (26.5%) were undergraduate dental students. The largest number of respondents, 140 (24.9%), were from the second year of study and 344 (60.9%) were from urban areas. The median total score was 20 and the interquartile range 4. The maximum possible score was 29. The scores among students belonging to different years of study were significantly different (p=0.006). Total scores were not significantly different among other subgroups.
CONCLUSIONS: The knowledge of the participants was good. Deficiencies in knowledge were noted in certain areas and these should be addressed through an educational intervention. One of the challenges is the rapid evolution of our knowledge about this condition, which may require regular refresher sessions. Similar studies can be undertaken in other medical colleges in the country and in nursing and pharmacy colleges.
AIM OF THE STUDY: Phytochemical investigation and assessment of pharmacological mechanism(s) involved in anti-ulcer effect of methanolic extract of the seeds of E. conferta.
MATERIALS AND METHODS: Bioactive phytoconstituents were isolated by column chromatography. These were identified by spectroscopic techniques including infrared (IR) spectroscopy, nuclear magnetic resonance (NMR) and mass spectrometry. Methanolic extract (MEC) of the seeds was prepared by cold maceration and its anti-ulcerogenic potential was evaluated using indomethacin (50 mg/kg) and water immersion stress models in male rats. The animals were pre-treated with different doses of MEC (400 and 800 mg/kg) and the therapeutic effect was compared with standard drug i.e. ranitidine (RANT; 50 mg/kg). The ameliorative effects of MEC were investigated on gastric juice pH, total acidity, free acidity and ulcer index. The assays of malionaldehyde (MDA), catalase (CAT), superoxide dismutase (SOD), glutathione (GSH) and pro-inflammatory cytokines i.e. interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were carried out to find out the possible mechanism(s) of protection. Further, histopathological changes were also studied.
RESULTS: Chromatography studies and further confirmation by spectroscopic techniques revealed the presence of four different compounds in MEC i.e oleic acid (1), stearic acid (2), ascorbic acid (3) and quercetin (4). MEC exhibited anti-ulcerogenic effect in dose dependent manner which may be attributed to suppression of pro-inflammatory cytokines (IL-6, TNF-α) and MDA (112.7%), and up-regulation of protective factors such as CAT (90.48%), SOD (92.77%) and GSH (90.01%). Ulcer inhibition, reduction in total and free acidity and increase in gastric juice pH were observed in MEC treated rats as compared to disease control animals. Histopathological findings confirmed decreased cell infiltration, less epithelial cell damage and regeneration of gastric mucosa in dose dependent manner.
CONCLUSIONS: The anti-ulcer effect of MEC may be attributed to its ability to scavenge free radicals and anti-inflammatory property via suppression of TNF-α and IL-6, thus offers a complete and holistic approach for management of peptic ulcer.
SUMMARY: Background Mutation of the growth factor-independent 1B (GFI1B) fifth DNA-binding zinc-finger domain causes macrothrombocytopenia and α-granule deficiency leading to clinical bleeding. The phenotypes associated with GFI1B variants disrupting non-DNA-binding zinc-fingers remain uncharacterized. Objectives To determine the functional and phenotypic consequences of GFI1B variants disrupting non-DNA-binding zinc-finger domains. Methods The GFI1B C168F variant and a novel GFI1B c.2520 + 1_2520 + 8delGTGGGCAC splice variant were identified in four unrelated families. Phenotypic features, DNA-binding properties and transcriptional effects were determined and compared with those in individuals with a GFI1B H294 fs mutation of the fifth DNA-binding zinc-finger. Patient-specific induced pluripotent stem cell (iPSC)-derived megakaryocytes were generated to facilitate disease modeling. Results The DNA-binding GFI1B variant C168F, which is predicted to disrupt the first non-DNA-binding zinc-finger domain, is associated with macrothrombocytopenia without α-granule deficiency or bleeding symptoms. A GFI1B splice variant, c.2520 + 1_2520 + 8delGTGGGCAC, which generates a short GFI1B isoform that lacks non-DNA-binding zinc-fingers 1 and 2, is associated with increased platelet CD34 expression only, without quantitative or morphologic platelet abnormalities. GFI1B represses the CD34 promoter, and this repression is attenuated by different GFI1B zinc-finger mutations, suggesting that deregulation of CD34 expression occurs at a direct transcriptional level. Patient-specific iPSC-derived megakaryocytes phenocopy these observations. Conclusions Disruption of GFI1B non-DNA-binding zinc-finger 1 is associated with mild to moderate thrombocytopenia without α-granule deficiency or bleeding symptomatology, indicating that the site of GFI1B mutation has important phenotypic implications. Platelet CD34 expression appears to be a common feature of perturbed GFI1B function, and may have diagnostic utility.