52 research outputs found
Irregular Meal Timing Is Associated with Helicobacter pylori
Background Helicobacter pylori (HP) is associated with chronic gastritis and gastric cancer, and more than half of the world’s population is chronically infected. The aim of this retrospective study was to investigate whether an irregular meal pattern is associated with increased risk of gastritis and HP infection. Methods The study involved 323 subjects, divided into three groups: subjects with HP infection and gastritis, with gastritis, and a control group. Subjects were interviewed on eating habits and meal timing. Multivariate logistic regression was used to compare groups. Adjusted odds ratios (OR) were derived controlling for gender, age, stress and probiotic consumption. Results Subjects who deviated from their regular meals by 2 hours or more had a significantly higher incidence of HP infection with gastritis (adjusted OR= 13.3, 95% CI 5.3–33.3, p<0.001) and gastritis (adjusted OR=6.1, 95% CI 2.5–15.0, p<0.001). Subjects who deviated their meals by 2 hours or more, twice or more per week, had an adjusted OR of 6.3 and 3.5 of acquiring HP infection with gastritis (95% CI 2.6–15.2, p<0.001) and gastritis (95% CI 1.5–8.5, p<0.001) respectively. Conclusion Frequent deviation in meal timing over a prolonged period appears associated with increased risk of developing HP infection and gastritis
The Safety of a Conservative Fluid Replacement Strategy in Adults Hospitalised with Malaria
BackgroundA conservative approach to fluid resuscitation improves survival in children with severe malaria; however, this strategy has not been formally evaluated in adults with the disease.MethodsAdults hospitalised with malaria at two tertiary referral hospitals in Myanmar received intravenous fluid replacement with isotonic saline, administered at a maintenance rate using a simple weight-based algorithm. Clinical and biochemical indices were followed sequentially.ResultsOf 61 adults enrolled, 34 (56%) had Plasmodium falciparum mono-infection, 17 (28%) Plasmodium vivax mono-infection and 10 (16%) mixed infection; 27 (44%) patients were at high risk of death (P. falciparum infection and RCAM score ≥ 2). In the first six hours of hospitalisation patients received a mean 1.7 ml/kg/hour (range: 1.3–2.2) of intravenous fluid and were able to drink a mean of 0.8 ml/kg/hour (range: 0–3). Intravenous fluid administration and oral intake were similar for the remainder of the first 48 hours of hospitalisation. All 61 patients survived to discharge. No patient developed Adult Respiratory Distress Syndrome, a requirement for renal replacement therapy or hypotension (mean arterial pressure < 60mmHg). Plasma lactate was elevated (> 2 mmol/L) on enrolment in 26 (43%) patients but had declined by 6 hours in 25 (96%) and was declining at 24 hours in the other patient. Plasma creatinine was elevated (> 120 μmol/L) on enrolment in 17 (28%) patients, but was normal or falling in 16 (94%) at 48 hours and declining in the other patient by 72 hours. There was no clinically meaningful increase in plasma lactate or creatinine in any patient with a normal value on enrolment. Patients receiving fluid replacement with the conservative fluid replacement algorithm were more likely to survive than historical controls in the same hospitals who had received fluid replacement guided by clinical judgement in the year prior to the study (p = 0.03), despite having more severe disease (p < 0.001).ConclusionsA conservative fluid resuscitation strategy appears safe in adults hospitalised with malaria
Fluctuations in Serum magnesium and Systemic Arterial Blood Pressures during the Menstrual Cycle in young reproductive women
Introduction: The menstrual cycle involves a sequence of structural, functional, and hormonal changes in the
reproductive system. This is linked and controlled by cyclical fluctuations in the levels of FSH, LH, estrogen,
and progesterone. Because of these cyclical fluctuations, there might also be associated cyclical changes of
magnesium and systemic arterial blood pressures during the menstrual cycle. Purpose: To assess the changes in
serum magnesium level and systemic arterial blood pressures during the menstrual cycle in young reproductive
women. Methodology: the sample population is 40 apparently healthy young reproductive-aged 18- 25years
female students from the University of Medicine, Magway participated in this study. Systemic arterial blood
pressures were measured by indirect method. The serum magnesium level was measured by spectrophotometry.
These measurements were done in the early follicular phase (EF), the peri-ovulatory phase (PO), and the midluteal phase (ML) of the menstrual cycle. The serum magnesium levels were significantly (p <0.001) lower, and
the systolic blood pressures were significantly higher (p <0.05) in the PO than the EF and the ML. In the EF,
there was a significant negative correlation between serum magnesium level and diastolic blood pressure (r= -
0.374, p <0.05) and mean arterial pressure (r = -0.354, p < 0.05) but no significant correlation with systolic blood
pressure. In the PO, there was no significant correlation between serum magnesium level and systemic arterial
blood pressures. In the ML, there was significant negative correlation between serum magnesium level and
systolic blood pressure (r = -0.651, p <0.001), diastolic blood pressure (r = -0.607, p <0.001), and mean arterial
pressure (r = -0.661, p <0.001). Conclusion: The study concludes that serum magnesium level has a negative
effect on blood pressure changes and the blood pressure-lowering effect of magnesium. These changes are
related to the fluctuation of estrogen levels during the menstrual cycle.
KEYWORDS: Serum magnesium, systemic arterial blood pressures, menstrual cycle reproductive syste
Do thrombotic events during endovascular interventions lead to poorer outcomes in patients with severe limb ischemia?
10.1177/1708538114546367Vascular233245-25
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LIS1 promotes the formation of activated cytoplasmic dynein-1 complexes.
Cytoplasmic dynein-1 is a molecular motor that drives nearly all minus-end-directed microtubule-based transport in human cells, performing functions that range from retrograde axonal transport to mitotic spindle assembly1,2. Activated dynein complexes consist of one or two dynein dimers, the dynactin complex and an 'activating adaptor', and they show faster velocity when two dynein dimers are present3-6. Little is known about the assembly process of this massive ~4 MDa complex. Here, using purified recombinant human proteins, we uncover a role for the dynein-binding protein LIS1 in promoting the formation of activated dynein-dynactin complexes that contain two dynein dimers. Complexes activated by proteins representing three families of activating adaptors-BicD2, Hook3 and Ninl-all show enhanced motile properties in the presence of LIS1. Activated dynein complexes do not require sustained LIS1 binding for fast velocity. Using cryo-electron microscopy, we show that human LIS1 binds to dynein at two sites on the motor domain of dynein. Our research suggests that LIS1 binding at these sites functions in multiple stages of assembling the motile dynein-dynactin-activating adaptor complex
LIS1 promotes the formation of activated cytoplasmic dynein-1 complexes.
Cytoplasmic dynein-1 is a molecular motor that drives nearly all minus-end-directed microtubule-based transport in human cells, performing functions that range from retrograde axonal transport to mitotic spindle assembly1,2. Activated dynein complexes consist of one or two dynein dimers, the dynactin complex and an 'activating adaptor', and they show faster velocity when two dynein dimers are present3-6. Little is known about the assembly process of this massive ~4 MDa complex. Here, using purified recombinant human proteins, we uncover a role for the dynein-binding protein LIS1 in promoting the formation of activated dynein-dynactin complexes that contain two dynein dimers. Complexes activated by proteins representing three families of activating adaptors-BicD2, Hook3 and Ninl-all show enhanced motile properties in the presence of LIS1. Activated dynein complexes do not require sustained LIS1 binding for fast velocity. Using cryo-electron microscopy, we show that human LIS1 binds to dynein at two sites on the motor domain of dynein. Our research suggests that LIS1 binding at these sites functions in multiple stages of assembling the motile dynein-dynactin-activating adaptor complex
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