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In our study, we aim to compare the resistance profiles of Acinetobacter baumannii and Pseudomonas aeruginosa isolates from intensive care unit (ICU) patients before and during the COVID-19 pandemic.
Materials:
The study involved adult patients monitored in the ICUs of a secondary-level hospital from January 2019 to December 2022. Isolates of A. baumannii and P. aeruginosa were obtained from blood, urine, and respiratory samples. Identification and antibiotic susceptibility tests were conducted using the disk diffusion method and the VITEK 2 system.
Results:
The average age of the patients was 61.3 ± 21.9 years (range: 18–95), with a majority of 1306 (51.6%) being male. During the pandemic, A. baumannii isolates showed a significant increase in resistance rates for several antibiotics compared to the pre-pandemic period: imipenem (96% vs 35.1%), amikacin (84.1% vs 14.4%), ciprofloxacin (96.9% vs 36.9%), trimethoprim-sulfamethoxazole (66.4% vs 27%), and ceftazidime (96.5% vs 33.3%) (all with P < .001). However, there was no significant change in colistin resistance rates in these isolates (0.9% vs 0%; P = .307). Similarly, Pseudomonas aeruginosa isolates exhibited significant increases in resistance rates during the pandemic compared to the pre-pandemic period: imipenem (51.5% vs 18.8%; P < .001), colistin (4.9% vs 0.6%; P = .009), amikacin (23.5% vs 4.4%; P < .001), ciprofloxacin (53.3% vs 13.8%; P < .001), and ceftazidime (39.2% vs 12.7%; P < .001).
Conclusion:
Our results demonstrate a significant increase in antibiotic resistance levels in Acinetobacter and Pseudomonas strains associated with hospital-acquired infections or colonization during the COVID-19 pandemic.
OBJECTIVES/SPECIFIC AIMS: According to the US census, there are 3.3 million Americans who have to use wheelchairs in order to maintain their mobility. About 50% of these patients develop a pressure ulcer at some point during their life time. Three major factors contribute to pressure ulceration; pressure, tissue temperature, and maceration due to sweating. The objective of this study is to develop a temperature regulating wheelchair cushion in order to address elevated tissue temperatures and related sweating. METHODS/STUDY POPULATION: We instrumented a wheelchair with cooling elements, a water filled cushion and a pump. The pump moves the water through the cooling elements where water temperature drops down to 15°C. The water then moves to the cushion where it cools the tissue and then back to the cooling elements. RESULTS/ANTICIPATED RESULTS: We recruited 1 healthy subject to sit on the instrumented wheelchair and then obtained thermographs of the cushion surface using an infrared thermal camera. After 1 minute of sitting on the cushion the minimum temperature was recorded as 27°C. After 10 minutes the temperature dropped to 23.3°C. DISCUSSION/SIGNIFICANCE OF IMPACT: In this ongoing proof-of-concept study we are investigating if circulating chilled water inside a wheelchair cushion is a feasible method to regulate tissue temperatures at the 25–28°C range. This range has been shown to delay ulceration under loading conditions that simulate sitting on a wheelchair. Initial results indicate that this may be an effective ulcer prevention method.
Many studies have evaluated patients with idiopathic hypogonadothropic hypogonadotropism (IHH), but few of these studies utilize event-related potentials (P300).
Aims:
To assess the cognitive functions of hypergonadotropic vs. hypogonadotropic patients.
Settings and design:
The study group consisted of 41 untreated IHH patients, 32 untreated Klinefelter syndrome (KS) patients, and 30 healthy control subjects.
Methods and material:
In this study, the latency and amplitude of P300 was evaluated in 41 untreated IHH and 32 untreated KS patients and compared to healthy control subjects (average age: 30 years). Also evaluated were the patients' hormone levels.
Results and conclusions:
In this study, the amplitude of P300 was found to be reduced, and the latency prolonged in IHH patients in comparison to KS patients and control subjects. In KS patients, there was no difference in latency of P300, but the amplitude was reduced when compared with the control group. Cognitive dysfunction in patients with hypogonadotropism is related to androgen hormone levels. This deficiency can affect development of the central nervous system (CNS), causing defects of CNS to varying degrees during the perinatal period. Androgen deficiency is considered to exert its effects during the period of cognitive ability development, manifest in IHH patients but not KS patients.
Objectives: Insulin-like growth factor-1 may serve some regulatory function in the immune system. Rheumatic mitral stenosis is related to autoimmune heart valve damage after streptococcal infection. The aim of this study was to assess the level of insulin-like growth factor-1 and its correlation with the Wilkins score in patients with rheumatic mitral stenosis. Methods: A total of 65 patients with rheumatic mitral stenosis and 62 age- and sex-matched control subjects were enrolled in this study. All subjects underwent transthoracic echocardiography. The mitral valve area and Wilkins score were evaluated for all patients. Biochemical parameters and serum insulin-like growth factor-1 levels were measured. Results: Demographic data were similar in the rheumatic mitral stenosis and control groups. The mean mitral valve area was 1.6±0.4 cm2 in the rheumatic mitral stenosis group. The level of insulin-like growth factor-1 was significantly higher in the rheumatic mitral stenosis group than in the control group (104 (55.6–267) versus 79.1 (23.0–244.0) ng/ml; p=0.039). There was a significant moderate positive correlation between insulin-like growth factor-1 and thickening of leaflets score of Wilkins (r=0.541, p<0.001). Conclusions: The present study demonstrated that serum insulin-like growth factor-1 levels were significantly higher in the rheumatic mitral stenosis group compared with control subjects and that insulin-like growth factor-1 level was also correlated with the Wilkins score. It can be suggested that there may be a link between insulin-like growth factor-1 level and immune pathogenesis of rheumatic mitral stenosis.
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