A comparison of HIV outpatient care in primary and secondary healthcare-level settings in Zimbabwe.

SETTING: Decentralisation of HIV care to nurse-led primary care services is being implemented across low- and middle-income countries in sub-Saharan Africa. OBJECTIVE: To compare services offered to clients attending for HIV care at a physician-led and a nurse-led service in Harare, Zimbabwe. DESIGN: A cross-sectional study was performed at Harare Central Hospital (HCH) and Budiriro Primary Care Clinic (PCC) from June to August 2018. An interviewer-administered questionnaire was used to collect sociodemographics, HIV treatment and clinical history from clients attending for routine HIV care. The Mann-Whitney U-test was used to evaluate for differences between groups for continuous variables. For categorical variables, the χ2 test was used. RESULTS: The median age of the 404 participants recruited was 38 years (IQR 28-47); 69% were female. Viral suppression was comparable between sites (HCH, 70% vs. PCC, 80%; P = 0.07); however, screening for comorbidities such as cervical cancer screening (HCH, 61% vs. PCC, 41%; P = 0.001) and provision of referral services (HCH, 23% vs. PCC, 13%; P = 0.01) differed between sites. CONCLUSION: Efforts to improve service provision in primary care settings are needed to ensure equity for users of health services.

(-)-Dioxosantadienic acid: hydrogen-bonding patterns in a bicyclic sesquiterpenoid keto acid and its monohydrate.

The anhydrous form, (I), of the title compound, (-)-2-(1,2,3,4,4a,7-hexahydro-4a,8-dimethyl-1,7-dioxo-2-naphthyl)propionic acid, C(15)H(18)O(4), derived from a naturally occurring sesquiterpenoid, has two molecules in the asymmetric unit, (I) and (I'), differing in the conformations of the saturated ring and the carboxyl group. The compound aggregates as carboxyl-to-ketone hydrogen-bonding catemers [O.O = 2.776 (3) and 2.775 (3) A]. Two crystallographically independent sets of single-strand hydrogen-bonding helices with opposite end-to-end orientation pass through the cell in the b direction, one consisting exclusively of molecules of (I) and the other entirely of (I'). Three C-H.O=C close contacts are found in (I). The monohydrate, C(15)H(18)O(4).H(2)O, (II), with two molecules of (I) plus two water molecules in its asymmetric unit, forms a complex three-dimensional hydrogen-bonding network including acid-to-water, water-to-acid, water-to-ketone, water-to-water and acid-to-acid hydrogen bonds, plus three C-H.O=C close contacts. In both (I) and (II), only the ketone remote from the acid is involved in hydrogen bonding.

(-)-3,6-Dioxo-5beta-cholanic acid: hydrogen bonding in the hemihydrate of a steroidal diketo acid.

The hemihydrate of the title diketo acid, C(24)H(36)O(4).0.5H(2)O, forms hydrogen-bonded carboxyl dimers related by a C(2) axis at crystallographic sites on the a and b edges of the chosen cell [O.O = 2.643 (7) and 2.716 (7) A]. The ketone ends of the molecules approach each other at sites near ((1/2),(1/2),(1/2)), ((1/2),0,(1/2)), (0,0,(1/2)) and (0,(1/2),(1/2)) in an interleaved arrangement incorporating partial-occupancy water hydrogen bonded to the B-ring ketone.

(+/-)-1-Tetralone-3-carboxylic acid and (+/-)-1-tetralone-2-acetic acid: hydrogen bonding in two gamma-keto acids.

The crystal structure of (+/-)-4-oxo-1,2,3,4-tetrahydronaphthalene-2-carboxylic acid (C(11)H(10)O(3)) involves projection of the carboxyl group nearly orthogonal to the aromatic plane and hydrogen bonding of the acid groups by centrosymmetric pairing across the a edge and the center of the chosen cell [O...O = 2.705 (2) A]. Intermolecular C--H...O==C close contacts to translationally related molecules are found for both the ketone (2.55 A) and the acid (2.67 A). In (+/-)-1-oxo-1,2,3,4-tetrahydronaphthalene-2-acetic acid (C(12)H(12)O(3)), the aggregation involves centrosymmetric carboxyl dimers mutually hydrogen bonded across the bc face and the a edge of the chosen cell [O...O = 2.674 (2) A]. A 2.60 A close C--H...O==C contact is found to the carboxyl group of centrosymmetrically related molecule.

(+)-Gibberellin C: hydrogen-bonding pattern of the monohydrate of a non-racemic pentacyclic diterpenoid.

In the monohydrate of the title compound, (+)-2beta, 4aalpha-dihydroxy-1,7-dimethyl-8-oxo-4bbeta,7alpha- gibbane-1alpha, 10beta-dicarboxylic acid-1,4a-lactone, C(19)H(24)O(6).H(2)O, intermolecular hydrogen bonding progresses helically along b from carboxyl to ketone [O...O = 2.694 (5) A]. The carboxyl and lactone carbonyl groups in translationally related molecules within a helix both accept hydrogen bonds from the same water of hydration. The oxygen of this water in turn accepts a hydrogen bond from the hydroxyl group of a third screw-related molecule in an adjacent counterdirectionally oriented helix, yielding a complex three-dimensional hydrogen-bonding array. Intermolecular O...H-C close contacts were found to the carboxyl and lactone carbonyls, the hydroxyl, and the water.

Pacing strategies during a cycling time trial with simulated headwinds and tailwinds.

The aims of this study were to examine the effects of one self-selected and two enforced pacing strategies (constant and variable power output) on cycling performance during a time trial in which variable wind conditions were simulated. Seven male cyclists rode their own bicycles on a Computrainer cycle ergometer, which was programmed to simulate a 16.1 km time trial on a flat course with a 8.05 km h(-1) headwind in the first half of the race and a 8.05 km h(-1) tailwind in the second half of the race. Subjects rode an initial time trial (ITT) at a self-selected pace to the best of their ability. The mean power output from this trial was then used to calculate the pacing strategies in the subsequent two trials: Constant (C)--riders rode the whole time trial at this mean power output; and Variable (V)--riders rode the first headwind section at a power output 5% higher than the mean and then reduced the power output in the last 8.05 km so that the mean power output was the same as in the initial time trial and in trial C. Power output, heart rate and ratings of perceived exertion (RPE) were recorded every 1.61 km. Finish times, 8.05 km split times and blood lactate levels, pre- and post-exercise (to calculate delta lactate), were also recorded in each trial. In the ITT, riders chose a mean +/- SD power output of 267 +/- 56 W in the first 1.61 km which was 14% higher than the overall race mean +/- SD of 235 +/- 41 W. Power outputs then dropped to below the race mean after the first few kilometres. Mean +/- SD finish times in the C and V time trials were 1661 +/- 130 and 1659 +/- 135 s, respectively. These were significantly faster than the 1671 +/- 131 s recorded in the initial time trial (p = 0.009), even though overall mean power outputs were similar (234 - 235 W) between all trials (p = 0.26). Overall mean RPE and delta lactate were lowest in trial V (p < 0.05). Perceived exertion showed a pacing strategy by race split interaction (p < 0.0001), but it was not increased significantly during the first 8.05 km of the V condition when power outputs were 5% higher than in condition C. Heart rate showed no main effect of pacing strategy (p = 0.80) and the interaction between strategy and race split did not reach statistical significance (p = 0.07). These results suggest that in a 16.1 km time trial with equal 8.05 km headwind and tailwind sections, riders habitually set off too fast in the first few kilometres and will benefit (10 s improvement) from a constant pacing strategy and, to a slightly greater degree (12 s improvement), from a variable (5% +/- mean) pacing strategy in line with the variations in wind direction during the race. Riders should choose a constant power when external conditions are constant, but when there are hilly or variable wind sections in the race, a variable power strategy should be planned. This strategy would be best monitored with 'power-measuring devices' rather than heart rate or subjective feelings as the sensitivity of these variables to small but meaningful changes in power during a race is low.

SPINK1/PSTI polymorphisms act as disease modifiers in familial and idiopathic chronic pancreatitis.

BACKGROUND & AIMS: Gain-of-function trypsin mutations cause acute pancreatitis and chronic pancreatitis. Loss of trypsin inhibitor function may have similar effects. We investigated the prevalence of SPINK1 (PSTI) mutations in familial pancreatitis, idiopathic chronic pancreatitis, and controls. METHODS: Genetic-linkage studies were performed in 5 familial pancreatitis families. The entire SPINK1 gene was sequenced in 112 affected individuals and 95 control DNA samples, and exon 3 was sequenced in 95 additional controls. X-ray crystallography-based model building and statistical studies were performed. RESULTS: Significant linkage between pancreatitis and 5q31.1-2 was excluded. Novel SPINK1 mutations, one D50E mutation, one IVS3+125 C>A, and five IVS3+184 T>A intronic polymorphisms were identified. The N34S and P55S mutations were observed in 29 of 112 patients (25%) as N34S/N34S (n = 7), N34S/wt (n = 19), N34S/P55S (n = 2), and N34S/D50E (n = 1). Three hundred eighty control alleles revealed 3 N34S (0.77%), 2 P55S (0.53%), and no D50E mutations. Age of disease onset and severity were similar between homozygous and heterozygous patients. Structural modeling revealed several possible pathophysiologic mechanisms for the N34S mutation. CONCLUSIONS: SPINK1 mutations are common in the population (approximately 2%), but are clearly associated with pancreatitis. The mutation-associated risk is low. Modeling and familial clustering suggest that SPINK1 mutations are disease modifying, possibly by lowering the threshold for pancreatitis from other genetic or environmental factors, but by themselves do not cause disease.

Antecedents of macrosomia.

Antecedents of high birthweight (macrosomia) were studied using the state birth certificates of White singleton infants born in three large metropolitan counties of Washington State from 1984 to 1986. Cases consisted of 2082 live-born macrosomic infants, defined by a birthweight of over 4.5 kg. A random sample of 4440 live births with birthweights of 2.5-4.0 kg was selected as a comparison group. Estimates for the independent risks associated with gestational and established diabetes, male sex, parity, duration of gestation, maternal smoking during pregnancy, maternal age, and median income of maternal residential area were obtained and combined in a single logistic model. Maternal smoking was associated with a decreased risk of macrosomia (OR 0.4, 95% CI 0.3-0.5). Established diabetes (OR 6.4, 95% CI 2.7-15.4), gestational diabetes (OR 3.2, 95% CI 2.1-5.1) and male sex of the infant (OR 2.4, 95% CI 2.2-2.7) were associated with an increased risk. Increasing parity was related to an increasing risk from para one (OR 1.4, 95% 1.2-1.6) to para six and greater (OR 3.3, 95% CI 1.5-7.4). Increasing duration of gestation was associated with an increasing risk from 33-36 weeks (OR 0.8, 95% CI 0.5-1.2) to 43-45 weeks (OR 3.3, 95% CI 2.5-4.2). Maternal age, median income of maternal area of residence, and maternal marital status were not significantly associated with macrosomia.

Some sources of error in the coding of birth weight.

Three types of error in coding birth weight to computer tapes are described: 1) confusion of ounces with pounds, 2) mistaken reading of one pound as eleven pounds, and 3) errors in placement of the decimal. All will allocate low birth weight infants to high birth weight categories. Examination of the reported gestational age of the infant or of the reported cause of death may allow these errors to be detected.