Early prediction of left ventricular function in streptokinase-treated acute myocardial infarction

We administered 750,000 units of intravenous streptokinase to 121 consecutive patients experiencing their first acute myocardial infarction within 4 h of pain onset. The following information was collected: hours between pain onset and streptokinase administration (TS), hours of pain after streptokinase administration (DP), initial and peak creatine phosphokinase levels (ICK and PCK), time to peak creatine phosphokinase, time to electrocardiographic ST segment resolution. Six days after the infarction, catheterization was performed to calculate ejection fraction, infarct-related regional ejection fraction, and dysfunction index. Data was analyzed using stepwise multiple regression. In patients experiencing anterior infarctions, the following equation was obtained predicting the ejection fraction (EF) with a correlation coefficient of 0.86: EF = 69 - 0.0050(PCK) - 3.7(TS) - 1.8(DP). In anterior infarctions the infarct-related ejection fraction and dysfunction index were similarly predictable. We were slightly less accurate in forecasting the outcome of inferior infarctions. The outcome of intravenous streptokinase therapy can be predicted early in the evolution of acute myocardial infarction using routinely available information.     

Parturition itself is the basis for fetal adrenal involution

CONTEXT: Newborn infants show a postnatal decline in androgen levels as the fetal adrenal glands involute. HYPOTHESIS: Placental factors up-regulate dehydroepiandrosterone sulfate (DHEA-S) generation. Hence, regardless of age, parturition will result in fetal adrenal involution and decline in DHEA-S levels. SUBJECTS AND METHODS: Premature neonates (n = 30) with gestational age 26-35 wk were studied. Adrenal volume by ultrasonography and serum DHEA-S, cortisol, and androstendione levels were followed weekly between d 1 and 28 of life. RESULTS: Serum DHEA-S was high on d 1 of life, declining rapidly regardless of gestational age during the first week of life (P < 0.001), and serum androstenedione and cortisol levels followed a similar pattern. Androstenedione levels showed a rise as of d 21 of life in boys but not in girls. The adrenals decreased in ultrasonographic volume from d 1 to 14 of life (P < 0.001), regardless of gestational age. CONCLUSIONS: Involution of the adrenal is faster than previously reported and, regardless of gestational age, occurs within the first week of life in terms of hormone secretion and within 2 wk in adrenal size. Involution involves a decline in DHEA-S but also in androstenedione and cortisol secretion, with a change in enzymatic activity. Males and females differ in their androstenedione levels and enzymatic activity. Parturition itself is the basis for fetal adrenal involution, supporting a key role for placental factors in maintaining the fetal adrenal and generating adrenal androgens.     

Overexpression of SOCS-2 and SOCS-3 genes reverses erythroid overgrowth and IGF-I hypersensitivity of primary polycythemia vera (PV) cells

Polycythemia vera (PV), an acquired, chronic, clonal disorder arising in a multipotential hematopoietic progenitor cell, is characterized by hyperplasia of three major myeloid lineages, with a pronounced increase in cells of the erythroid lineage. Erythroid progenitor cells in PV are strikingly hypersensitive to insulin-like growth factor-I (IGF-I); this effect is specific and is mediated through the IGF-I receptor. To investigate the possibility that in PV the increase in number of erythroid progenitors and their hypersensitivity to IGF-I result from a defect in negative regulation of cytokine activity, we examined the expression of members of the SOCS gene family. Circulating mononuclear cells, grown in serum-free methylcellulose medium in the presence of IGF-I, produced BFU-E-derived colonies whose cells revealed a reduction of SOCS-2 and SOCS-3 expression in PV only. Overexpression of these genes in transfected PV cells reduced their erythroid overgrowth and IGF-I hypersensitivity. We hypothesize that a defect in expression of SOCS-2 and SOCS-3 genes may be crucial for the IGF-I hypersensitivity and progressive increase in erythroid cell population size characteristic of PV.     

Phosphorylation of HOX11/TLX1 on Threonine-247 during mitosis modulates expression of cyclin B1

Background  

The HOX11/TLX1 (hereafter referred to as HOX11) homeobox gene was originally identified at a t(10;14)(q24;q11) translocation breakpoint, a chromosomal abnormality observed in 5-7% of T cell acute lymphoblastic leukemias (T-ALLs). We previously reported a predisposition to aberrant spindle assembly checkpoint arrest and heightened incidences of chromosome missegregation in HOX11-overexpressing B lymphocytes following exposure to spindle poisons. The purpose of the current study was to evaluate cell cycle specific expression of HOX11.     

Autoimmune Esophagitis: IgG4-related Tumors of the Esophagus

We present a case of a 23-year-old gentleman who presented with dysphagia, weight loss, and recurrent esophageal strictures requiring multiple dilatations. An endoscopic ultrasound with esophagogastroduodenoscopy revealed a mass present in the distal esophagus. Fine needle aspiration suggested that the mass in the lower esophagus resembled a gastrointestinal stromal tumor. After surgical resection, final pathologic analysis revealed that the tumor was comprised of benign-appearing fibroinflammatory cells with an increase and predominance of IgG4-positive plasma cells. The microscopic appearance was consistent with a benign condition as a result of an IgG4-related process. He did not, however, have any other symptoms indicative of systemic autoimmune disease or connective tissue disorders. We present the pre-operative imaging, operative management, pathologic diagnosis, and literature review of this rare condition and the first known report of autoimmune esophagitis as part of the IgG4 spectrum of diseases.     

Bromocriptine treatment of hyperprolactinemic infertility with ovulatory disturbances

We studied 77 women with hyperprolactinemic infertility and possible ovulatory disturbances. Galactorrhea was present in 27. Ovulation was normal in 15, 21 were anovulatory and 41 had luteal phase deficiency. All patients received bromocriptine for three months, resulting in normal serum prolactin levels. After that time, if no pregnancy occurred, clomiphene (with or without human chorionic gonadotropin) or human menopausal gonadotropin and human chorionic gonadotropin were added to the treatment. The overall pregnancy rate was 65%. The incidence of hyperprolactinemia in infertile patients is higher than expected, and patients with luteal phase deficiency can benefit from treatment with bromocriptine and ovulatory agents.