Risk factors for brachial plexus injury and permanent sequelae due to shoulder dystocia.

Aim: The primary aim of this study was to determine the risk factors for the occurrence of brachial plexus injury in cases of shoulder dystocia. Secondly, it was aimed to determine the factors affecting the occurrence of permanent sequelae in cases with brachial plexus injury. Subjects and Methods: ICD-10 codes were scanned from the records of patients who gave birth between 2012 and 2018, and the records of patients with brachial plexus injury and shoulder dystocia were reached. Shoulder dystocia cases with brachial plexus damage were accepted as the study group, and shoulder dystocia cases without brachial plexus damage were considered the control group. Shoulder dystocia patients with brachial plexus injury and without injury were compared for 2-year orthopedics clinic follow-up reports, surgical intervention, permanent sequelae status as well as birth data, maternal characteristics, and maneuvers applied to the management of shoulder dystocia. Results: Five hundred sixty births with shoulder dystocia were detected. Brachial plexus injury was observed in 88 of them, and permanent sequelae were detected in 12 of these patients. Maneuvers other than McRobert's (advanced maneuvers) were used more and clavicle fracture was seen more in the group with plexus injury (P < 0.05, P < 0.05, respectively). Logistic regression analysis was performed to determine the risk factors of brachial plexus injury. Brachial plexus injury was observed 4.746 times more in infants who were delivered with advanced maneuvers and 3.58 times more in infants with clavicle fractures at birth. Conclusion: In patients with shoulder dystocia, the risk of brachial plexus injury increased in deliveries in which advanced maneuvers were used and clavicle fracture occurred.

Effect of synbiotics in the treatment of smokers and non-smokers with gingivitis: randomized controlled trial.

BACKGROUND: To evaluate the efficacy of synbiotic tablets on the clinical and biochemical parameters of smokers and non-smokers with gingivitis. METHODS: Eighty patients with gingivitis [40 smokers (+), 40 non-smokers (-)] were randomly assigned to test (T) or control (C) groups. Four groups were defined: T(+), T(-), C(+) and C(-). The subjects daily chewed a synbiotic or placebo tablet for 30 days. The gingival crevicular fluid levels of interleukin (IL)-6, IL-8 and IL-10 were determined as the primary outcome variables. RESULTS: The clinical and biochemical parameters for all groups significantly reduced compared with the baseline (P < 0.05). While there were no significant differences between the groups for gingival index, the plaque index was significantly higher in both smoker groups than that in the T(-) group during the second month (P < 0.05). IL-8 levels in C(-) and IL-6 levels in both control groups were significantly higher than those in the T(+) group. The IL-10 levels in both control groups were significantly higher than those in the T(-) group during the second month (P < 0.05). CONCLUSIONS: Adjunctive synbiotic tablets significantly reduce subclinical therapeutic outcomes for both smokers and non-smokers compared with placebo according to the biochemical parameters.

Determination of serum adenosine deaminase and xanthine oxidase activity in Kangal dogs with maternal cannibalism.

AIM: Kangal dogs, known as guard dogs in many countries of the world, have been found to eat their own puppies during their first 24 h following birth, which is called as maternal cannibalism. Adenosine deaminase (ADA) and xanthine oxidase (XO) are important enzymes for purine metabolism. In this study, the aim is to evaluate ADA and XO activities in Kangal dogs with maternal cannibalism. MATERIALS AND METHODS: The material of the study consists of the blood sera of Kangal dog breed with and without maternal cannibalism in the breeders around Sivas city and its districts. ADA and XO activities in blood serum of these animals were investigated by spectrophotometric method. RESULTS: ADA activities in Kangal dogs with maternal cannibalism were increased to the control group without maternal cannibalism (p<0.01). CONCLUSION: Postnatal measurement of ADA activity in dogs may be useful in assessing maternal cannibalism.

Higher P-wave dispersion in migraine patients with higher number of attacks.

OBJECTIVE AND AIM: An imbalance of the sympathetic system may explain many of the clinical manifestations of the migraine. We aimed to evaluate P-waves as a reveal of sympathetic system function in migraine patients and healthy controls. MATERIALS AND METHODS: Thirty-five episodic type of migraine patients (complained of migraine during 5 years or more, BMI < 30 kg/m²) and 30 controls were included in our study. We measured P-wave durations (minimum, maximum, and dispersion) from 12-lead ECG recording during pain-free periods. ECGs were transferred to a personal computer via a scanner and then used for magnification of x400 by Adobe Photoshop software. RESULTS: P-wave durations were found to be similar between migraine patients and controls. Although P WD (P-wave dispersion) was similar, the mean value was higher in migraine subjects. P WD was positively correlated with P max (P < 0.01). Attacks number per month and male gender were the factors related to the P WD (P < 0.01). CONCLUSIONS: Many previous studies suggested that increased sympathetic activity may cause an increase in P WD. We found that P WD of migraine patients was higher than controls, and P WD was related to attacks number per month and male gender. Further studies are needed to explain the chronic effects of migraine.

Prenatal diagnosis of diastematomyelia in a 15-week-old fetus.

OBJECTIVE: A case of prenatal diagnosis of diastematomyelia is presented. METHODS: A case of fetal diastematomyelia, diagnosed by prenatal sonography, demonstrated the typical sonographic features of this condition. In this case it was detected at 15 weeks of gestation, and presented with a midline echogenic focus in the posterior region of the thoracolumbar spine. RESULTS: The pregnancy was terminated by induction of labor. The fetus was female and there was a 1-cm long endurated hyperemic lesion at the back of the fetus. We confirmed the diagnosis of diastematomyelia after termination of pregnancy by plain chest and abdominal X-ray and also MRI scanning. CONCLUSION: Isolated diastematomyelia is a rare form of spinal dysraphism characterized by a sagittal cleft in the spinal cord, conus medullaris and/or filum terminale with splaying of the posterior vertebral elements. Prenatal diagnosis of this anomaly is possible in the early mid-trimester by sonography, thus allowing for early surgical intervention and a favorable prognosis.

Allosteric regulation of liver phosphorylase a: revisited under approximated physiological conditions.

Phosphorylase removes glucosyl units from the terminal branches of glycogen through phosphorolysis, forming glucose-1-P. It is present in two interconvertible forms, phosphorylase a and b. The a form is the active form and is rate limiting in glycogen degradation. The activities of phosphorylase a and of total phosphorylase as conventionally measured exceed the activities of glycogen synthase R (active form) and of total synthase by approximately 10- and 20-fold. Thus, unless phosphorylase a is inhibited or compartmentalized or its substrates are exceedingly low in vivo, net glycogen synthesis could not occur. In addition, following an administered dose of glucose, phosphorylase a activity changes little when glycogen is being synthesized, is stable, or is being degraded, suggesting an important role for allosteric effectors in regulation. Therefore, we have determined the effect of potential modifiers of enzyme activity at estimated intracellular concentrations. Purified liver phosphorylase a was used. Activity was measured in the direction of glycogenolysis, at 37 degrees C, pH 7.0, and under initial rate conditions. Both a Km and a near-saturating concentration of inorganic phosphate (substrate) were used in the assays. A physiological concentration of AMP was saturating. It decreased the Km for Pi by approximately 50% and stimulated activity. ADP, ATP, and glucose inhibited activity. Fructose-1-P inhibited activity only at a high and nonphysiological concentration. Glucose-6-P and UDP-glucose were not significant inhibitors. Inhibition of activity by ADP was little affected by the addition of AMP. However, AMP partially abolished the inhibitory effect of ATP and completely abolished the inhibitory effect of glucose. When AMP, ADP, ATP, glucose-6-P, UDP-glucose, glucose, and fructose-1-P were added together, the net effect was no change in phosphorylase a activity compared to the activity without any effectors. In addition, changes in glucose concentration did not affect activity. K glutamine modestly stimulated activity. Numerous other metabolites were tested and were without effect. The present data indicate that the known endogenous allosteric effectors cannot explain the smaller than expected in vivo phosphorylase a activity or the regulation of phosphorylase a activity.

Effects of glucagon with or without insulin administration on liver glycogen metabolism.

Rats fed ad libitum were given insulin alone (4 U/kg), glucagon alone (25 micrograms/kg), or insulin and glucagon sequentially. Phosphorylase a and synthase R activities, hepatic glycogen, uridine diphosphoglucose, inorganic phosphate (Pi), and plasma glucose, lactate, glucagon, and insulin concentrations were determined over the subsequent 40 min. In separate animals, muscle extraction of 2-deoxy-D-[3H]glucose also was determined. After glucagon administration, glycogen phosphorylase a and plasma glucose were increased within 5 min. However, the glycogen concentration did not decrease for 20 min. Glucagon administration to rats pretreated with insulin stimulated a similar increase in phosphorylase a activity. Again, glycogen was not degraded for 20 min. After insulin only, glycogen concentration remained unchanged. Plasma glucose decreased as expected. In each group, muscle extraction of 2-deoxy-D-[3H]glucose increased compared with the controls (P < 0.05). In summary, glucagon and/or insulin administration did not stimulate significant glycogen degradation for 20 min, even though phosphorylase was activated. The mechanism remains to be determined.

Effect of added fat on the plasma glucose and insulin response to ingested potato given in various combinations as two meals in normal individuals.

OBJECTIVE: In normal subjects, ingestion of fat with potato in a morning meal resulted in a decrease in the glucose response. Therefore, we wished to determine whether a fat-induced decrease in blood glucose also would be observed after a second identical meal. In addition, we were interested in determining if fat ingestion with a morning meal would have an effect on the blood glucose and insulin responses to a second meal not containing fat. RESEARCH DESIGN AND METHODS: Nine healthy male subjects ingested two meals consisting of an amount of potato containing 50 g carbohydrate, either alone or with 50 g fat as butter. The meals were served in four combinations as follows: 1) potato for the first meal, potato for the second meal; 2) potato for the first meal, potato with fat for the second meal; 3) potato with fat for the first meal, potato for the second meal; and 4) potato with fat for the first meal, potato with fat for the second meal. Meals were ingested at 8:00 A.M. and noon. Plasma glucose and C-peptide, serum insulin, triglyceride, and free fatty acid (FFA) concentrations were determined over an 8-h period. The integrated area responses to the meals were quantified over the subsequent 4-h period using the fasting value or the noon value as baseline for the first and second meals, respectively. RESULTS: When the first meal contained potato only, the glucose area response to the second meal was significantly less when the second meal contained fat. However, fat ingestion had no effect on the glucose area response to the second meal when fat was present in the first meal. The insulin area responses to the first and second meals were similar after ingestion of potato or potato with fat. However, the insulin response to the second meal always was less than that to the first meal. The C-peptide area responses after ingestion of the second meal also were all higher than those after the first meal. The triglyceride area responses were slightly negative after ingestion of potato alone in the first meal. When fat was ingested, they were positive. When the first meal contained fat but the second meal did not, there was a rise in triglyceride concentration after the second meal as well as after the first meal. That is, a rise occurred without ingestion of fat with the second meal. If fat was present in the second meal the rise was even greater. The FFA area responses were similar to the triglyceride area responses. CONCLUSIONS: When fat was ingested with carbohydrate in either the first or second meal, the glucose area response was decreased. However, when both meals contained fat, a decrease in the glucose area response did not occur with the second meal. The glucose area responses all were greater after the second meal compared with those after the first meal, i.e., the opposite of a Staub-Traugott effect was observed. The insulin area responses to the first and second meals were similar whether fat was ingested or not.

Liver glycogen synthase, phosphorylase, and the glycogen concentration in rats given a glucose load orally: a 24-hour study.

Fasted rats were given 4 g/kg glucose orally. Synthase R (active forms), total synthase, and phosphorylase alpha activities, and hepatic glycogen, glucose 6-phosphate (glucose-6P), uridine diphosphoglucose (UDP-glucose), glucose, and plasma glucose concentrations were determined over the subsequent 24 h. The resulting glycogen concentration changes could be divided into three distinct phases. A glycogen synthetic phase (between 0 and 4 h), a stability phase (between 4 and 12 h), and a degradation phase (between 12 and 24 h). Synthase R activity increased rapidly and reached a maximum at 20 min. With the onset of glycogen synthesis it gradually decreased below the control values, reaching a nadir by 4 h. During the glycogen stability phase it gradually increased again up to the control value. It then remained stable during the subsequent glycogen degradation phase. Phosphorylase a activity did not change throughout the entire 24-h period. Glucose-6-P concentration increased almost twofold at 20 min. It then decreased but was above the control values at the 24th h. The plasma and hepatic glucose concentrations increased as expected after the glucose load. They then decreased but remained above the control value at all subsequent time points. In summary, the synthase R, phosphorylase a activities, or changes in the known allosteric modifiers of these enzymes could not explain the changes in glycogen concentration. The reasons for these discrepancies remain to be determined.

Incorporation of glycogenin into a hepatic proteoglycogen after oral glucose administration.

Glycogenin is a 37-kDa protein upon which new glycogen molecules are considered to be constructed. Therefore, we were interested in determining its role in liver glycogen synthesis following glucose administration. Twenty-four-hour fasted rats were given 4 g/kg glucose orally. Glycogenin and synthase R activities and glycogen were determined over the subsequent 24 h. In fasted rats given just water, glycogenin activity was present and did not change over the subsequent 24 h. Following glucose, glycogenin activity also was not different for 1 h, i.e. the glycogenin was not incorporated into glycogen even though the glycogen concentration had increased. Subsequently, the glycogenin activity became unmeasurable. Presumably, the glycogenin was incorporated into a proteoglycan product since after amylase treatment, glycogenin activity was again present and was quantitatively unchanged. Free glycogenin activity remained unmeasurable until after 12 h. At this time, glycogen began to decrease, and, by 15 h, free glycogenin activity again appeared. The results indicate that in fasted rats, essentially all of the glycogenin was free. Following administration of oral glucose, glycogenin was incorporated into a proteoglycan product but only 60 min after glycogen synthesis had begun. Free glycogenin did not reappear until the 15th h after glucose was given and after the glycogen concentration had decreased by approximately 60%.

Effects of glucose, galactose, and lactose ingestion on the plasma glucose and insulin response in persons with non-insulin-dependent diabetes mellitus.

Galactose usually is ingested as lactose, which is composed of equimolar amounts of glucose and galactose. The contribution of galactose to the increase in glucose and insulin levels following ingestion of equimolar amounts of galactose and glucose, or lactose, has not been reported in people with non-insulin-dependent diabetes mellitus (NIDDM). Therefore, we studied the effects of galactose ingestion alone, as well as with glucose either independently or in the form of lactose, in subjects with untreated NIDDM. Eight male subjects with untreated NIDDM ingested 25 g glucose, 25 g galactose with or without 25 g glucose, or 50 g lactose as a breakfast meal in random sequence. They also received 50 g glucose on two occasions as a reference. Water only was given as a control meal. Plasma galactose, glucose, glucagon, alpha-amino nitrogen (AAN), nonesterified fatty acids (NEFA), and serum insulin and C-peptide concentrations were determined over a 5-hour period. The integrated area responses were quantified over the 5-hour period using the water control as a baseline. Following ingestion of 25 g galactose, the maximal increase in plasma galactose concentration was 1 mmol/L. The mean maximal increases in plasma galactose concentration following ingestion of 25 g galactose + 25 g glucose or following 50-g lactose meals were similar and were only 12% of that following ingestion of galactose alone (P < .05). The mean galactose area response over the water control for the 25-g galactose meal was 0.95 +/- 0.31 mmol.h/L.(ABSTRACT TRUNCATED AT 250 WORDS)

Plasma glucose and insulin responses to bananas of varying ripeness in persons with noninsulin-dependent diabetes mellitus.

With progressive ripeness there is a decrease in starch and an increase in free sugar content of bananas. The starch also is considered to be poorly digestible. Therefore, we decided to study plasma glucose, serum insulin, C-peptide, and plasma glucagon responses to bananas with increasing degrees of ripeness. Seven male subjects with untreated noninsulin-dependent diabetes mellitus ingested 50 g carbohydrate as bananas of stage 4 (more yellow than green), 5 (yellow with green tip), 6 (all yellow), and 7 (yellow flecked with brown) ripeness. They also received 50 glucose on two occasions for comparative purposes. On a separate occasion water only was given as a control. The area responses were quantified by determining incremental areas using the water control as baseline. The mean glucose area following the 50 g glucose meals was 15.1 +/- 1.9 mM.h. After the ingestion of bananas of 4, 5, 6 and 7 ripeness the glucose area response was 42, 41, 51 and 48% of that after glucose ingestion, respectively. The insulin area response following glucose meals was 888 pM.h. Responses to 4, 5, 6 and 7 bananas were 85, 70, 61, 85%, respectively, of that following glucose ingestion. C-peptide data were similar to the insulin data. The glucagon area response was negative after glucose ingestion but was positive following banana ingestion. In summary, the glucose, insulin, C-peptide, and glucagon area responses varied little with ripeness of the bananas.

Effect of added fat on plasma glucose and insulin response to ingested potato in individuals with NIDDM.

OBJECTIVE: In normal subjects, ingestion of butter with potato resulted in considerably lower blood glucose levels but similar or higher insulin concentrations compared with those observed in the same subjects after potato ingestion alone. We determined whether butter ingested with potato would result in a greater stimulation in insulin secretion than ingestion of potato alone in subjects with NIDDM. RESEARCH DESIGN AND METHODS: Seven male subjects with untreated NIDDM ingested 50 g CHO alone or 50 g CHO with 5, 15, 30, or 50 g fat as a breakfast meal. Fat was ingested in the form of butter, and CHO was given in the form of potato. Subjects received 50 g glucose on two separate occasions for comparative purposes. The subjects also were given only water and were studied over the same time period (water control). Plasma glucose, glucagon, alpha-amino nitrogen, nonesterified fatty acids, serum insulin, C-peptide, and triglyceride concentrations were determined over 5 h. The integrated area responses were quantified over the 5-h period using the water control as a baseline. RESULTS: The mean plasma glucose area response after ingestion of potato with or without the various amounts of butter were all similar and were 82% of that observed after ingestion of 50 g glucose. The mean insulin area response to potato alone was 532 pmol.h.L-1. The mean insulin area responses to potato plus 5,15,30, and 50 g of fat meals were 660,774,750, and 756 pmol.h.L-1, respectively. Thus, the mean insulin areas were all greater than for ingestion of potato alone, and a maximal response was observed with addition of 15 g fat (1.4-fold). The C-peptide data did not confirm an increase in insulin secretion. Overall the area responses after ingestion of meals containing fat were not different from the response to potato ingestion alone, although the responses were erratic. The glucagon area response was positive after ingestion of all fat containing meals except for that containing only 5 g fat, and there was a dose-response relationship. The plasma alpha-amino nitrogen and nonesterified fatty acid area responses were negative after potato ingestion and were not significantly different when fat was added. The serum triglyceride concentration increase was greater after the ingestion of butter with the potato as expected. CONCLUSIONS: In contrast to the results in normal subjects after ingestion of butter with potato, the glucose response was not smaller in subjects with NIDDM. The insulin response was greater. The insulin area response data indicated the presence of a dose-response relationship. Whether similar responses will be observed with other dietary fat and CHO sources remains to be determined.