Poor quality of sleep and musculoskeletal pains among highly trained and elite athletes in Senegal.

BACKGROUND: Previous studies reported that poor sleep quality (PSQ) was associated with musculoskeletal pains (MSP) and poor physical performance in athletes. OBJECTIVE: The current study aimed at determining PSQ and its associations with MSP in some sub-Saharan athletes. METHODS: A cross sectional study was conducted among 205 highly trained and 115 elite athletes (aged: 25 ± 2 years, Body mass index: 22.8 ± 0.9 kg/m2) in Dakar, Senegal, during a competitive season in a variety of sport disciplines including athletics, basketball, football, rugby, wrestling, tennis. Quality of sleep and MSP were assessed using the French version Pittsburgh Sleep Quality Index (PSQI) and French version of Nordic questionnaire respectively. Pain on body joints during a week was defined as seven-day MSP (MSP-7d) and PSQ for a PSQI > 5. RESULTS: 27.8% (95%CI: 23.2-32.9) of the overall sample suffered PSQ, with 33.7% (95%CI: 24.7-44.0) in basketball and 24.7% (95%CI: 16.9-34.6) in football. According to athletic status and gender, PSQ was more prevalent among highly trained (66.3; 95%CI: 55.9-75.3) and men (69.7%; 95%CI: 59.5-78.7). Among athletes with PSQ 43.8% (95%CI: 33.9-54.2) suffered MSP-7d, with 36.6%; highly trained (95%CI: 23.7-42.9) and 28.1% female. Considering body region, hips/thigh (14.6%; 95% CI: 8.74-23.4) and upper back (13.5%; 95%CI: 7.88 -21, 1) were more affected. Basketball players were more affected from MSP (MSP-7d = 38.5%; 95%CI: 24. 9-54.1) on high on wrists/hands (MSP-7d = 44.4%; 95%CI: 18.9 -73.3; P = 0.04). Based on athletic status, MSP-7d were higher on highly trained necks (100%; 95%CI: 56.1-100; p = 0.04). PSQ was associated with basketball (OR: 3.062, 95%CI: 1.130-8.300, p = 0.02) compared to Athletic. PSQ and MSP-7d were associated on Wrist/hands (OR: 3.352, 95%CI: 1.235-9.099, p = 0.01), and at the upper back (OR: 5.820, 95%CI: 2.096-16.161, p = 0.0007). CONCLUSION: These results indicate that PSQ is considerable among Senegalese athletes and is associated with MSP during a week. Hence, we recommend to look for strategies optimizing good quality of sleep in order to reduce pains, to improve health.

[Ischemic gangrene of the upper limb associated with COVID-19 infection: about 2 cases]. / Gangrène ischémique du membre supérieur corrélée à l'infection de la COVID-19: à propos de 2 cas.

Clinical manifestations of COVID-19 have changed a lot, ranging from respiratory and Ear, Nose and Throat (ENT) symptoms to extra pulmonary thrombotic, neurological, cardiac and renal complications. We here report the case of two patients with SARS-CoV-2 pneumonia whose course was marked by prolonged upper limb ischemia. The association between venous, but also arterial, thrombotic complications and viral infection is now well established, and appears to be related to hypercoagulability.

Musculoskeletal pains among amateur and professional athletes of five disciplines in Senegal: a preliminary study.

BACKGROUND: Musculoskeletal pains (MSPs) in sport are cause of poor performances and loss of competition in athletes. The present study aimed at determining the prevalence of MSPs with regard to sport disciplines and athletic status. METHODS: A cross-sectional study was conducted among 320 Senegalese professional and amateur athletes practicing football, basketball, rugby, tennis, athletics, and wrestling. Rates of MSPs in the past year (MSPs-12) and week (MSPs-7d) were assessed using standard questionnaires. RESULTS: Overall proportions of MSPs-12 and MSPs-7d were 70 and 74.2%, respectively. MSPs-12 were more frequently reported on shoulders (40.6%), neck (37.1%) and hips/thigh (34.4%), while MSPs-7d were predominant on hips/thigh (29.5%), shoulders (25.7%), and upper back (17.2%). Proportions of MSPs-12 and MSPs-7d varied significantly by sport disciplines, with highest values among basketball players. Again, highest MSPs-12 proportions on shoulders (29.7%, P = 0.02), wrists/hands (34.6%, P = 0.001), (40.2%, P = 0.0002), and knees (38.8%, P = 0.002) were seen among basketball players. High proportions of MSPs-7d were seen on shoulders (29.6%, P = 0.04) for tennis players, wrists/hands (29.4%, P = 0.03) for basketball and football players, and hips/thigh (38.8%, P < 0.00001) for basketball players. Football players had reduced risk of MSPs-12 by 75% on lower back (OR = 0.25; 95% CI. 0.10-0.63; P = 0.003) and by 72% on knees (OR = 0.28; 95% CI. 0.08-0. 95; P = 0.04). In contrast, tennis players were more at risk of MSPs-12 on shoulders (OR = 3.14; 95% CI. 1.14-8.68; P = 0.02), wrists/hands (OR = 5.18; 95% CI.1.40-11.13; P = 0.01), and hips/thigh (OR = 2.90; 95% CI. 1.1-8.38; P = 0.04). Professionals were protected from MSPs-12 on neck pain with a significant reduction of risk by 61% (OR = 0.39, 95% CI. 0.21-0.75, P = 0.03). CONCLUSION: MSPs are a reality among athletes and their risk is modulated by sport disciplines, athletic status and gender.

Impact of the interaction between the polymorphisms and hypermethylation of the CD36 gene on a new biomarker of type 2 diabetes mellitus: circulating soluble CD36 (sCD36) in Senegalese females.

BACKGROUND: Several predisposing factors for diabetes mellitus have been identified, including cluster determinant 36 (CD36) receptor expression. We aimed to determine the effects of CD36 gene polymorphisms and hypermethylation on the plasma CD36 protein levels in type 2 diabetes. MATERIALS AND METHODS: We conducted a cross-sectional study involving 100 females (lean healthy control subjects and subjects with type 2 diabetes). This study was conducted at the Human Physiology Laboratory at the Dakar Faculty of Medicine in Senegal. Circulating sCD36 levels and DNA methyltransferase 3a levels were determined by enzyme-linked immunosorbent assay. The other biological parameters were evaluated in a biochemical laboratory. CD36 gene polymorphisms and methylation were explored by real-time polymerase chain reaction and methylation-specific polymerase chain reaction, respectively. RESULTS: sCD36 was negatively correlated with HDL-cholesterol levels (r = - 0.52 p = 0.0001) and triglyceride levels (r = - 0.36 p = 0.01) in control subjects. However, in the type 2 diabetes group, sCD36 levels were positively correlated with total cholesterol levels (r = 0.28 p = 0.04). For rs3211867, control subjects harboring the CC genotypes had significantly higher sCD36 levels than control subjects harboring the AA/AC genotype (p = 0.02); in the type 2 diabetes group, the sCD36 level was not significantly lower in subjects harboring the AA/AC genotype than in subjects harboring the CC genotype (p = 0.27). CD36 gene methylation reduced the sCD36 level in the control subjects compared to control subjects without CD36 gene methylation (p = 0.03). This difference was not significant in the type 2 diabetes group comparing subjects with diabetes with CD36 gene methylation to subjects with diabetes without CD36 gene methylation (p = 0.09). We noted a nonsignificant increase in sCD36 levels in subjects with diabetes with CD36 gene methylation compared to control subjects with CD36 gene methylation (p = 0.27). A combination of the CD36 polymorphism effect and the CD36 methylation effect did not significantly reduce sCD36 levels in subjects with type 2 diabetes. CONCLUSION: CD36 gene polymorphisms and CD36 gene methylation separately reduce sCD36 levels. Their impacts are compensated for in subjects with type 2 diabetes by an increase in sCD36 levels, the mechanism of which needs to be elucidated.

Frequencies and Distribution of APOE Gene Polymorphisms and Its Association With Lipid Parameters in the Senegalese Population.

Background Apolipoprotein E is a multifunctional protein that plays an important role in lipid metabolism. It is encoded by the APOE gene. However, APOE gene polymorphism has not been very well studied in the Senegalese population. Therefore, we studied allele frequencies, genotype distributions, and the relationship between APOE gene polymorphisms and lipid parameters in the Senegalese women population. Methodology This study included 110 healthy women aged 35-72 years. The mean age was 49.8 ± 8.1 years. For all subjects, lipid parameters were analyzed from fasting serum, and APOE genotypes were identified by PCR-RFLP (polymerase chain reaction-restriction fragment length polymorphism) based analysis. Results Variations in the frequencies and distribution of the APOE alleles and genotypes were observed (ε3: 47.3%; ε2: 43.2%; ε4: 9.6%; and ε2/ε3: 70%; ε2/ε4: 16.4%; ε3/ε3: 10.9%; ε2/ε4: 2.7%). Compared to the ε3ε3 genotype carriers, carriers of the ε3ε4 genotype had a significantly higher rate of total cholesterol (p=0.03) and no high-density lipoprotein-cholesterol (p=0.02). Univariate analysis showed that the APOE ε4 allele increases the low-density lipoprotein-cholesterol rate (OR=3.06; 95% CI: 1.16-8.22; p=0.02). Conclusion Our study has shown a difference in APOE allele frequencies and genotype distributions with a total absence of ε2ε2 and ε4ε4 genotypes in a sample of Senegalese women. We also found that APOE gene polymorphism might play a role in plasma lipid levels.

Evaluation of Bonding Quality with Advanced Nondestructive Testing (NDT) and Data Fusion.

This work aims to compare quantitatively different nondestructive testing (NDT) techniques and data fusion features for the evaluation of adhesive bonding quality. Adhesively bonded composite-epoxy single-lap joints have been investigated with advanced ultrasonic nondestructive testing and induction thermography. Bonded structures with artificial debonding defects in three different case studies have been investigated: debonding with release film inclusion, debonding with brass film-large, debonding with brass film-small. After completing preprocessing of the data for data fusion, the feature matrices, depending on the interface reflection peak-to-peak amplitude and the principal component analysis, have been extracted from ultrasonic and thermography inspection results, respectively. The obtained feature matrices have been used as the source in basic (average, difference, weighted average, Hadamard product) and statistical (Dempster-Shafer rule of combination) data fusion algorithms. The defect detection performances of advanced nondestructive testing techniques, in addition to data fusion algorithms have been evaluated quantitatively by receiver operating characteristics. In conclusion, it is shown that data fusion can increase the detectability of artificial debonding in single-lap joints.

Pulse wave velocity is lower in trained than in untrained sickle cell trait carriers.

BACKGROUND: Sickle cell trait (SCT) is a benign condition of sickle cell disease. Nevertheless, previous reports showed that SCT carriers have increased blood viscosity and decreased vascular reactivity compared to non-SCT carrier. The benefit of regular exercise on vascular function has been well documented in the general population but no study focused on the SCT population. PURPOSE: The aim of our study was to compare arterial stiffness and blood viscosity between trained and untrained SCT carriers, as well as a group of untrained non-SCT. METHODS: Arterial stiffness (finger-toe pulse wave velocity) and blood viscosity were evaluated in untrained non-SCT carriers (n = 10), untrained SCT carriers (n = 23) and trained SCT carriers (n = 17) who reported at least 10 hours of physical exercise per week. RESULTS: Untrained SCT carriers had higher pulse wave velocity (p = 0.032) and blood viscosity (p < 0.001) than their trained counterparts. In addition, untrained SCT carriers had higher blood viscosity (p < 0.001) than the untrained non-SCT group. A positive association was noted between blood viscosity and pulse wave velocity in the whole study population. CONCLUSION: Our study suggests that regular exercise may be beneficial for the vascular function of SCT carriers.

Alcohol and thiamine deficiency trigger differential mitochondrial transition pore opening mediating cellular death.

Accumulating evidence has shown that binge-type alcohol intake in mothers interferes with thiamine deficiency (TD) to promote the fetal alcohol syndrome (FAS). Developmental alcohol or TD exposures act either synergistically or separately to reproduce FAS features e.g. intrauterine growth retardation and related microcephaly characterized by extensive cellular death induced by one another neurotoxicant. However molecular and cellular mechanisms underlying apoptosis in both alcohol and TD toxicities are unknown. The current review addresses mechanisms of apoptosis underlying alcohol and TD toxicities for further understanding FAS pathology. This study indicates two different mitochondria pathways regulating cellular death: The first mechanism may engage alcohol which activates the c-subunit ring of the F0-ATP synthase to form MPT pore-dependent apoptosis; following the second mechanism, TD activates CyP-D translocation from mitochondrial matrix towards the mitochondrial inner membrane to form MPT pore-dependent necrosis. These studies shed light upon molecular and cellular mechanisms underlying apoptosis and necrosis in developemental brain disorders related to alcohol and thiamine deficiency, in hopes of developing new therapeutic strategies for FAS medication.

Soft porous silicone rubbers with ultra-low sound speeds in acoustic metamaterials.

Soft porous silicone rubbers are demonstrated to exhibit extremely low sound speeds of tens of m/s for these dense materials, even for low porosities of the order of a few percent. Our ultrasonic experiments show a sudden drop of the longitudinal sound speed with the porosity, while the transverse sound speed remains constant. For such porous elastomeric materials, we propose simple analytical expressions for these two sound speeds, derived in the framework of Kuster and Toksöz, revealing an excellent agreement between the theoretical predictions and the experimental results for both longitudinal and shear waves. Acoustic attenuation measurements also complete the characterization of these soft porous materials.

Cardiopulmonary response to exercise in COPD and overweight patients: relationship between unloaded cycling and maximal oxygen uptake profiles.

Cardiopulmonary response to unloaded cycling may be related to higher workloads. This was assessed in male subjects: 18 healthy sedentary subjects (controls), 14 hypoxemic patients with chronic obstructive pulmonary disease (COPD), and 31 overweight individuals (twelve were hypoxemic). They underwent an incremental exercise up to the maximal oxygen uptake (VO2max), preceded by a 2 min unloaded cycling period. Oxygen uptake (VO2), heart rate (HR), minute ventilation (VE), and respiratory frequency (fR) were averaged every 10 s. At the end of unloaded cycling period, HR increase was significantly accentuated in COPD and hypoxemic overweight subjects (resp., +14 ± 2 and +13 ± 1.5 min(-1), compared to +7.5 ± 1.5 min(-1) in normoxemic overweight subjects and +8 ± 1.8 min(-1) in controls). The fR increase was accentuated in all overweight subjects (hypoxemic: +4.5 ± 0.8; normoxemic: +3.9 ± 0.7 min(-1)) compared to controls (+2.5 ± 0.8 min(-1)) and COPDs (+2.0 ± 0.7 min(-1)). The plateau VE increase during unloaded cycling was positively correlated with VE values measured at the ventilatory threshold and VO2max. Measurement of ventilation during unloaded cycling may serve to predict the ventilatory performance of COPD patients and overweight subjects during an exercise rehabilitation program.

Soft porous silicone rubbers as key elements for the realization of acoustic metamaterials.

In this work, macroporous materials made of polydimethylsiloxane, a soft silicone rubber, are prepared using UV polymerization with an emulsion-templating procedure. The porosity of the final materials can be precisely controlled by adjusting the volume of the dispersed phase. We show that the porous structure of the materials is the template of the droplets of the initial emulsions. Mechanical tests show that the materials Young's moduli decrease with the porosity of the materials. Acoustic measurements indicate that, in such a porous elastomeric matrix, the sound speed also decreases dramatically as soon as the porosity increases to attain values of as low as 80 m/s. The results are compared to earlier ones on silica aerogels and are interpreted within the framework of a simple theoretical approach. We show that the very low sound speed value is a consequence of the low value of the polymer shear modulus. This explains why such porous soft silicone rubbers are so efficient at playing the role of slow-soft resonators in acoustic metamaterials. Moreover, the fast rate of polymerization of such UV-curable fluid allows for a facile shaping of the final material as beads or rods in microfluidic devices.1.

Effects of hydration and water deprivation on blood viscosity during a soccer game in sickle cell trait carriers.

The present study compared the changes in blood viscosity, hydration status, body temperature and heart rate between a group of sickle cell trait (SCT) carriers and a control (Cont) group before and after a soccer game performed in two conditions: one with water offered ad libitum (hydration condition; Hyd) and the other one without water (dehydration condition; Dehyd). Blood viscosity and haematocrit per blood viscosity ratio (HVR; an index of red blood cell oxygen transport effectiveness) were measured before and at the end of each game. Resting blood viscosity was greater in the SCT carriers than in the Cont group. The increase of blood viscosity over baseline at the end of the game in the Cont group was similar in the two conditions. In contrast, the change in blood viscosity occurring in SCT carriers during soccer games was dependant on the experimental condition: (1) in Dehyd condition, blood viscosity rose over baseline; (2) in Hyd condition, blood viscosity decreased below resting level reaching Cont values. The Cont group had higher HVR than SCT carriers at rest. HVR remained unchanged in the Cont group at the end of the games, whatever the experimental condition. Although HVR of SCT carriers decreased below baseline at the end of the game performed in Dehyd condition, it increased over resting level in Hyd condition reaching the values of the Cont group. Our study demonstrated that ad libitum hydration in exercising SCT carriers normalises the blood hyperviscosity.

Intraday blood rheological changes induced by Ramadan fasting in sickle cell trait carriers.

The goal of the present study was to test whether fasting during the holy period of Ramadan may disturb blood rheology in sickle cell trait (SCT) carriers more than in a group of subjects with normal hemoglobin. Twenty African male students participated in the study: 10 SCT carriers and 10 subjects with normal hemoglobin (CONT). Biochemical parameters (plasma glucose and lipids levels), hematocrit, blood viscosity, and urine specific gravity were measured in the two groups on the 14th day of the Ramadan period (Ramadan condition) and 6 wks after the end of Ramadan (baseline condition). All the measurements were performed twice for each experimental day to measure intraday variation: 8:00 and 18:00 h. Plasma glucose level and lipid profile were not significantly different between the two groups. Although Ramadan did not affect the lipid profile, the plasma glucose concentration was lower during the Ramadan period compared with the baseline condition in the two groups. Hematocrit and urine specific gravity did not differ between the two groups and was greater in the evening than in the morning, independently of the condition. SCT carriers had higher blood viscosity than the CONT group. However, whereas blood viscosity remained unchanged through the day in the CONT group, whatever the condition, SCT carriers were characterized by a large increase of blood viscosity in the evening during the Ramadan period, indicating higher risk for microcirculatory blood flow impairments. Specific medical recommendations are needed for SCT carriers engaged in religious fasting.

Perinatal thiamine deficiency-induced spontaneous abortion and pup-killing responses in rat dams.

OBJECTIVES: The current study attempts to determine whether thiamine (B1 vitamin) deficiency and chronic alcohol-related thiamine-deficient (TD) status, disturb maternal behavior towards pups. METHODS: During gestation and lactation, Wistar rat dams were exposed to the following treatments: (i) prenatal TD dams; (ii) perinatal TD dams; (iii) postnatal TD dams; (iv) 12% alcohol/water drinking mothers; (v) ad libitum control dams. Pair-feeding treatments controlled malnutrition related to thiamine deficiency; (vi) prenatal pair-fed (PF) dams; (vii) perinatal PF dams; (viii) postnatal PF dams and included also the control of alcohol consummation: (ix) PF saccharose dams. Dams were observed for gestation outcome and for apparent disorders of the maternal behavior related to the pups at parturition. RESULTS: From the nine experimental groups studied, only pre- and perinatal TD dams exhibited spontaneous abortion (33.36 and 41.66%, respectively) followed by pups-killing responses where, respectively, 4 dams/7 (57.14%) and 5 dams/7 (71.43%) showed disruption of maternal behavior and appearance of cannibalism towards pups which all were killed within 48 hours after parturition. Spontaneous abortion and pup-killing responses were not observed in the dams of any other experimental group, suggesting that perinatal disturbances of hormonal factors underlay these maternal disorders. DISCUSSION: Previous studies reported that thiamine deficiency-induced degeneration of dopamine neurons may be related to mouse-killing aggression in rats. The present study suggests that perinatal thiamine deficiency-induced alteration of dopaminergic neurons in maternal brain could be a trigger factor of pup-killing responses. Central dopamine and oxytocin have been strongly associated with both the onset and maintenance of maternal behavior and the regulation of maternal aggressiveness as well. Our studies suggest that estrogen control oxytocin levels in brain structures of pregnancy-terminated rats via dopamine transmission. Thiamine may modulate cAMP/Ca2+ -dependent estradiol-triggered responses which in turn control dopamine synthesis. Consequently, thiamine deficiency induced perinatally triggers pup-killing responses in pregnancy-terminated rats by the following toxic effects: (i) disturbances of estrogen production and/or release affecting dopamine synthesis; (ii) alterations of dopamine inhibition on central oxytocinergic system-related maternal aggressiveness. Likewise, our results indicate also that perinatal thiamine deficiency alone induces spontaneous abortion, reduces litter size, and lowers birth weight, which together suggest changing in the fetoplacental estrogen receptor alpha/progesterone receptor A ratio during gestation, via autocrine/paracrine regulation disturbances. Those hypotheses should be confirmed by further investigations.

Effects of thiamine deficiency on food intake and body weight increment in adult female and growing rats.

The present study compared the effects of thiamine (vitamin B1) deficiency (TD) on the patterns of food intake and body weight in adult female and neonatal Wistar rats. The adults weighed 250-270 g at the start and were fed for 60 days either with a synthetic TD diet (211 B1) or with the same synthetic diet+thiamine (210 B1). TD led to a marked reduction in food intake and the body weight set point, both recovering rapidly to their initial level in only 3 days after dietetic reversion. The effects of TD in developing rats were evaluated by subjecting pregnant rats to thiamine restriction during different time windows: prenatal (3 days before mating to parturition); perinatal (7 days after mating to the 10th postnatal day); and postnatal (from parturition to weaning). The effect of TD on the occurrence of low birth weight and ponderal growth retardation was examined from postnatal days 1 to 45. Only perinatal TD significantly decreased birth weight relative to untreated or pair-fed controls. Moreover, compared with the control treatments, ponderal growth retardation was not induced by prenatal TD, whereas induction of TD from perinatal into postnatal periods did cause ponderal growth retardation, with long-lasting effects persisting in adulthood. The results suggest a major physiological role of thiamine in the homeostasis of body weight programming, increment, and set point regulation in both offspring and adult female rats.

Paradoxical effects of alcohol and thiamine deficiency on the eye opening in rat pups.

OBJECTIVE: The present study attempts to determine whether developmental thiamine (B1 vitamin) deficiency and developmental ethanol exposure disturb eye opening in Wistar rat pups. METHODS: During gestation and lactation, Wistar rat dams were exposed to the following treatments: (1) Prenatal thiamine-deficient dams; (2) perinatal thiamine-deficient dams; (3) postnatal thiamine-deficient dams; (4) 12% alcohol/water drinking mothers; (5) mothers drinking 12% alcohol/water + thiamine hydrochloride mixture; (6) ad libitum control dams. Pair-feeding treatments controlled malnutrition related to thiamine deficiency: (7) Prenatal pair-fed dams; (8) perinatal pair-fed dams; (9) postnatal pair-fed dams and included also the control of alcohol consummation: (10) pair-fed saccharose dams. After birth, from postnatal day 10 (P10) to P18, eye opening was observed in the pups bred by ten different experimental dams. RESULTS: The present experiments showed eye opening to be delayed strongly in perinatal thiamine-deficient pups only. Consequently, our study suggests perinatal thiamine deficiency to interfere with photoreceptors differentiation in the rat retina. In addition, our results reveal that developmental alcohol exposure-induced premature eye opening contrasted paradoxically with perinatal thiamine deficiency-induced delayed opening. CONCLUSIONS: The results suggest differential actions of alcohol and thiamine deficiency on cellular genesis in the rat retina.

Comparative effects of alcohol and thiamine deficiency on the developing central nervous system.

The present study addresses the still unresolved issue of the character of alcohol-thiamine metabolic interferences in the developing central nervous system (CNS). Investigations compare developmental neurotoxicity evoked by three patterns of maternal thiamine deficiency (pre, peri and postnatal), with two patterns of maternal chronic alcohol intake (alcohol alone and alcohol+thiamine cotreatment), on seven neurodevelopmental abilities in the offspring. The three patterns of thiamine deficiency, pair-compared with controls, highlight four sequences of development: (1) embryonic-perinatal sequence; (2) perinatal-postnatal sequence; (3) "ontogeny in ontogeny out" sequence; (4) "off and on" developing sequence. The results suggest a temporally- and regionally emergence of structures and centers underlying functional maturation during CNS ontogenesis. Furthermore, both developmental thiamine deficiencies and ethanol exposure produce two waves of neurofunctional alterations, peaking at P15 (postnatal day 15) and P25, respectively. The first peak of vulnerability is a prenatal event; it may interfere with the periods of intense cellular proliferation and migration. The second peak represents both perinatal and postnatal events; it may interfere with the periods of cellular differentiation, synaptogenesis, axonogenesis and myelinogenesis. Alcohol+thiamine cotreatment fails to reduce the first peak, but neutralizes essentially the second peak. The results suggest that alcohol interferes with thiamine during cellular differentiation and membrane developmental processes mainly. Indeed, among the three conditions of thiamine-deficient diet, only perinatal thiamine deficiency exhibits a closer relationship with developmental alcohol exposure. Together, these observations suggest that the critical period for alcohol-thiamine antagonism occurs perinatally and affects primarily cellular differentiation.

Alcohol and B1 vitamin deficiency-related stillbirths.

OBJECTIVE: The present study attempts to determine whether prenatal thiamine (B1 vitamin) deficiency and prenatal alcohol exposure are risk factors for stillbirths. METHODS: From conception to parturition, Wistar rat dams were exposed to the following treatments: (1) Rat dams consuming a thiamine-deficient diet; (2) 12% alcohol/water drinking mothers; (3) mothers drinking 12% alcohol/water + thiamine hydrochloride mixture. Appropriate pair-fed controls and ad libitum controls were assessed. Gestation outcome and fetal parameters, including spontaneous abortion, still-born fetuses, litter size and birth weight, were assessed from the dams of each experimental group. RESULTS: Both alcohol and thiamine deficiency during pregnancy increased fetal death (48.26%vs. 84.47%), reduced litter size (44.54%vs. 72.7%), respectively, and lowered birth weight. Thiamine administration reversed the effects of alcohol-induced fetal death, suggesting that a part of deleterious actions of alcohol on fetal death was mediated by thiamine deficiency. Prenatal thiamine deficiency increased singularly spontaneous abortion with abundant bleeding (40%), rising the occurrence of stillbirth. Such a pathology was not observed in alcohol group. CONCLUSIONS: The results indexed thiamine deficiency as a potent risk factor for stillbirths. The vitamin supply during pregnancy prevents stillbirths related to chronic alcoholism and different facets of malnutrition.

Post-exercise heart rate recovery in healthy, obeses, and COPD subjects: relationships with blood lactic acid and PaO2 levels.

Because blood acidosis and arterial oxygenation (PaO(2)) play key roles in the chemoreflex control of cardiac activity, we hypothesized that heart rate (HR) decay rate after maximal exercise may be linked to post-exercise increase in blood lactate (LA) level and/or the resting PaO(2). Twenty healthy subjects and thirty five patients at risks of cardiovascular diseases (20 obeses; 15 patients with chronic obstructive pulmonary disease, COPD) performed a maximal cycling exercise. During the recovery period, HR was continuously measured for consecutive 10-s epochs allowing to compute linear or second order polynomial equations and to calculate every minute HR variations compared to peak HR value (DeltaHR). PaO(2) was measured at rest and post-exercise maximal LA level was determined. A second order polynomial equation (y = a(2) x (2) + b(2) x + c) best fitted the post-exercise HR decay rate. The a(2) and b(2) coefficients and DeltaHR did not depend on age, sex, and body mass index. Despite a large scattering of HR decay rate, even present in healthy subjects, a(2) and DeltaHR were significantly lower in obeses and COPDs. In the whole population, both a(2) coefficient and DeltaHR were negatively correlated with maximal post-exercise LA level. DeltaHR was lowered in hypoxemic patients. Thus, the slowest post-exercise HR decay rate was measured in subjects having the highest peak LA increase or hypoxemia. Thus, even in healthy subjects, the post-exercise HR decay rate is lowered in individuals having an accentuated exercise-induced LA increase and/or hypoxemia. The mechanisms of delayed post-exercise HR recovery are only suspected because significant correlations cannot assess cause-to-effect relationships.

Metabolic and structural role of thiamine in nervous tissues.

In the literature, previous descriptions of the role of thiamine (B1 vitamin) focused mostly on its biochemical functions as a coenzyme precursor of some key enzymes of the carbohydrate metabolism. This report reviews recent developments on the metabolic and structural role of thiamine, e.g., the coenzyme and noncoenzyme functions of the vitamin. Taking into account analysis of our experimental data relating to the effects of thiamine deficiency on developing central nervous system (CNS) and data available in literature, we seek to establish a clear difference between the metabolic and structural role of thiamine. Our experimental data indicate that the specific and nonspecific effects express two diametrically diverse functions of thiamine in development: the nonspecific effects show up the metabolic consequences of thiamine deficiency resulting in apoptosis and severe cellular deficit; inversely, the specific effects announced the structural consequences of thiamine deficiency, described as cellular membrane damage, irregular and ectopic cells. The review highlights the existence of noncoenzyme functions of this vitamin through its interactions with biological membranes.