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N Magid

Publications and source records attributed to N Magid.

10 recordsLinked to original sources

Diabetes teratogenicity in mice is accompanied with distorted expression of TGF-beta2 in the uterus.

Early embryonic deaths as well as malformed newborns are among complications of the diabetic pregnancy. Cytokines and growth factors operating in the embryonic vicinity are found to be among factors that determine the sensitivity of embryos to external and internal detrimental stimuli, including diabetes. Transforming Growth Factor-beta2 (TGF-beta2) has been shown to be essential for embryonic development and survival. In the present work, we evaluated the pattern of TGF-beta2 expression in the uterus of streptozotocin-induced diabetic mice, demonstrating a decreased reproductive performance and elevated percentage of litters with severely malformed fetuses. Since stimulation of the maternal immune system was found to increase the resistance of mouse embryos to the teratogenic effect of diabetes, the effect of immunopotentiation on the expression of the cytokine was also investigated. TGF-beta2 expression was studied at the mRNA level by using the in situ hybridization technique and at the protein level by using the immunohistochemical analysis. A clear decrease in TGF-beta2 mRNA expression in the uterus of diabetic mice was observed at examined time points: days 1, 5, and 9 of pregnancy. Also, an evident reduction in TGF-beta2, the protein expression in the uterus of diabetic mice, was demonstrated at these time points. Maternal immunopotentiation that improved the reproductive performance of diabetic mice and reduced the number of the litters with malformed fetuses was also accompanied by a clear increase in the level of TGF-beta2 mRNA expression in the pregnant uteri. The above results clearly demonstrate that the embryotoxic effect of diabetes is accompanied by an alteration of TGF-beta2 expression. Immunopotentiation that was shown to improve the reproductive performance of the diabetic mice was accompanied by a partial normalization of TGF-beta2 expression in embryonic vicinity.

Animals↗

Midgut volvulus in infants: diagnosis with US. Work in progress.

The authors present findings from ultrasound (US) studies that can alert sonologists to the possibility of midgut malrotation complicated by volvulus in neonates and infants. A fluid-filled, distended duodenum seen at US examination in infants is a nonspecific sign of duodenal obstruction, as well as one of the signs of midgut malrotation. In addition, dilated, thick-walled bowel loops, mainly to the right of the spine, and peritoneal fluid were found at abdominal US examinations of three infants with midgut malrotation complicated by volvulus. In one infant with uncomplicated midgut malrotation, only signs of duodenal obstruction were present. The findings at US of duodenal obstruction associated with thickened bowel loops to the right of the spine and peritoneal fluid should lead the sonologist to suspect midgut malrotation complicated by volvulus, a potentially fatal condition, and an upper gastrointestinal series should then be performed to confirm the diagnosis.

Duodenal Obstruction↗

Role of lipoxygenase in the mechanism of acrosome reaction in mammalian spermatozoa.

The acrosome reaction (AR) in bull spermatozoa was induced by the Ca2(+)-ionophore A23187, by dilauroylphosphatidylcholine or by arachidonic acid in the presence of Ca2+ in the incubation medium. The occurrence of AR was determined by following the release of acrosin from the cells. Nordihydroguaiaretic acid (NDGA), an inhibitor of both lipoxygenase and prostaglandin-synthetase, caused 35%, 43% and 69% inhibition of AR at concentrations of 1, 10 or 100 microM, respectively. Eicosatetraynoic acid (ETYA), an analogue of arachidonic acid, caused 17%, 61% and 77% inhibition of AR at concentrations of 20, 40 or 80 micrograms/ml, respectively. When AR was induced by arachidonic acid, ETYA, causes 36% and 58% inhibition at concentrations of 2 or 20 micrograms/ml, respectively. Under identical conditions, 100 microM indomethacin, a specific inhibitor of prostaglandin-synthetase, showed no inhibition but rather 35% stimulation at acrosin release rate. The fact that AR is inhibited by NDGA and not by indomethacin indicates that the lipoxygenase, rather than prostaglandin-synthetase, is involved in the mechanism of AR. Since the inhibition by NDGA is seen in the presence of the Ca-ionophore, we suggest that lipoxygenase activity is not involved in enhancing calcium transport into the cell, but rather at other steps in AR mechanism. A thin-layer chromatography revealed the presence of 15-HETE, the classical product of 15-lipoxygenase activity, which was identified by HPLC. Under AR conditions, there is an elevation of lipoxygenase products and the addition of NDGA caused a reduction in their levels. The inhibition of acrosin release by NDGA can be eliminated by adding 15-HETE or 15-HPETE to the incubation medium. In conclusion, we suggest here for the first time, a physiological role for 15-lipoxygenase in the mechanism of AR in mammalian spermatozoa.

5,8,11,14-Eicosatetraynoic Acid↗

A "hole in a rib" as a sign of child abuse.

Cyst-like radiolucencies ("holes") in ribs can be a manifestation of many different abnormalities. Two cases of child-abuse are presented in which the initial clue leading to the diagnosis of a battered-child was a cyst-like lytic lesion in the posterior rib cage.

Bone Cysts↗

Low heart rate variability and sudden cardiac death.

Our results indicate the following. 1. HRV is markedly depressed in inducible SCD survivors, a group at high risk of a subsequent episode of SCD. 2. Studies on patients who developed SCD during Holter monitoring indicate that HRV is depressed prior to SCD. 3. HRV is markedly depressed in inducible "asymptomatic ventricular ectopy" patients, with the degree of reduction paralleling that observed in inducible SCD survivors. In contrast, HRV of noninducible "asymptomatic ventricular ectopy" patients did not differ statistically from normal. 4. The findings provide additional evidence that cardiac parasympathetic function is depressed in patients prone to development of SCD and that altered autonomic function contributes to the development of electrical instability in such individuals. This accords with findings that such risk factors for sudden death as coronary artery disease, myocardial infarction, congestive failure, and hypertension all have been associated with reduced parasympathetic activity or attenuation of parasympathetically mediated reflexes. It is tempting to believe that diminished cardiac parasympathetic activity, perhaps by failing to counter excess sympathetic activity, contributes to SCD. 5. It may be inferred that HRV measurements have potential for serving as an independent predictor of inducibility in response to programmed ventricular stimulation and that they could represent a noninvasive screen for patients referred for evaluation of risk of SCD because of asymptomatic ventricular ectopy or other causes. In a larger sense, the data suggest that HRV measurements may provide information pertinent to the identification of individuals at increased risk of SCD that is independent of that provided by other risk factors. Given the human and economic stakes, further study is clearly warranted.

Death, Sudden↗

Respiratory illness and hypophosphatemia.

We retrospectively reviewed the charts of 308 admissions to a pulmonary disease ward and 100 admissions to the general medical service over one year to find the prevalence, sequelae, and etiology of hypophosphatemia. The overall prevalence of low serum phosphate levels (less than 2.4 mg/dl) occurring at least once during hospitalization in chest patients was 17 percent, but was higher in patients with respiratory infections (28 percent). Moreover, the prevalence of hypophosphatemia on admission (before institution of intravenous fluid or drug therapy) was ten times higher in patients with respiratory infections than in patients with noninfectious respiratory illness or general medical patients (21 vs 2 percent, p less than 0.001). Serum phosphate less than 2.0 mg/dl occurred in 4 percent of patients. Twenty-seven percent of the patients (including two with ventilatory failure) with abnormally low serum phosphate levels had symptoms or signs of uncertain etiology later explicable by the presence of hypophosphatemia. The most common additional laboratory finding associated with hypophosphatemia was elevation of muscle enzymes. Although mortality was no higher in hypophosphatemic patients, hospital stay was twice as long as that of patients with normal levels of serum phosphate. No correlation was found between simultaneous arterial blood gases and serum phosphate levels. Two patients given antacids had severe hypophosphatemia and worsened ventilatory function; phosphate-binding antacids should be used judiciously in patients with severe respiratory disease, since they may lead to the development or worsening of hypophosphatemia and diminished ventilatory function.

Female↗

Antimyosin antibody imaging in experimental aortic regurgitation.

BACKGROUND: Fiber dropout and myocyte necrosis precede heart failure in experimental aortic regurgitation (AR). The current study aimed to determine whether this process can be detected by noninvasive scintigraphic imaging. METHODS AND RESULTS: 111In-labeled antimyosin antibody Fab fragment (1 to 1.5 mCi) (Myoscint) was administered to each of 34 New Zealand White rabbits: 11 early (3 to 5 weeks) after surgical AR induction; 9 late (98 to 128 weeks) after AR induction; 5 normal and 3 sham-operated age-matched with early AR; and 3 normal and 3 sham-operated age-matched with late AR. Echocardiographic fractional shortening was indistinguishable among control, early AR, and late AR groups. In vivo gamma camera imaging 24 and 48 hours after isotope administration, post-mortem heart activity determination (percentage injected dose per gram), and autoradiography were performed. At 24 and 48 hours, heart-to-lung counts-per-pixel ratios from in vivo images were greater (p < 0.05) in the late AR rabbits than in each of the three other groups. No significant differences were found when early AR and older or younger control rabbits were compared. Heart activity (percentage injected dose per gram) in late AR rabbits trended toward higher values than in age-matched control rabbits (p = 0.057), but in early AR it was indistinguishable from that in the corresponding control (p = 0.413, difference not significant). The autoradiographic endocardial/epicardial activity ratio in late AR rabbits was greater than in control and early AR rabbits (1.27 +/- 0.13 vs 1.06 +/- 0.09 and vs 1.13 +/- 0.10, respectively, p < 0.02). CONCLUSIONS: Whereas isotope uptake in late AR rabbits differed from that in control and early AR rabbits, systolic function was indistinguishable. Thus 111In-labeled antimyosin antibody imaging may permit noninvasive detection of AR-induced myocardial damage before functional deterioration.

Animals↗

Left ventricular function of heart allografts during acute rejection: an echocardiographic assessment.

Left ventricular function was evaluated in nine patients during biopsy proven acute rejection of heart allografts using computer-assisted analysis of echocardiograms. The results were compared with data obtained during their non-rejection state and with data obtained from 10 normal subjects. Left ventricular dimensions and parameters of diastolic and systolic function of non-rejecting hearts were similar to those of normals. Acute rejection was associated with increased left ventricular mural thickness and mass, and abnormal diastolic function characterized by a prolongation of the rapid filling period from 155 msec +/- 14 msec to 183 msec +/- 16 msec (p less than 0.05, mean +/- SE), and decreased normalized peak rates of left ventricular lengthening (from 5.3 sec-1 +/- 0.8 sec-1 to 3.9 sec-1 +/- 0.4 sec-1, less than 0.05) and posterior wall thinning (from 7.4 sec-1 +/- 1.0 sec-1 to 3.8 sec-1 +/- 0.6 sec-1, p less than 0.05). Parameters of systolic function as defined by fractional shortening, peak normalized rates of left ventricular shortening and posterior wall thinning were not altered by acute rejection. We conclude that the left ventricular function of non-rejecting hearts is similar to that of normals; however, acute rejection is associated with abnormal left ventricular diastolic dynamics without adverse effect on systolic function.

Adult↗