Purpose. Premature ovarian failure occurs in 40%-70% of patients who receive conventional chemotherapy alone. However, the incidence is higher, 70%-100%, in patients who undergo myeloablative chemotherapy with hematopoietic stem cell transplantation (HSCT). Gonadotropinreleasing hormone (GnRH) analogs, such as leuprolide, in a continuous-release formulation, may protect the ovaries from the gonadotoxic effects of chemotherapy. In non-HSCT settings, GnRH analogs have reduced the risk for premature ovarian failure to <10%. We conducted a phase II clinical trial based on the hypothesis that giving leuprolide before conditioning chemotherapy in HSCT patients reduces premature ovarian failure incidence.Patients and Methods. Eligible patients were women aged <40 years who were HSCT candidates, were premenopausal, and had both follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels <20 IU/L. Two 22.5-mg leuprolide doses were delivered in 3-month depot i.m. injections, the first within 2 months before HSCT. Patients were monitored for menstruation return, and ovarian function tests (FSH, LH, and estradiol) were done every 2 months starting 90 days after the last leuprolide dose.Results. Sixty eligible patients were enrolled, 59 underwent HSCT, and 44 were evaluable (median age, 25 years; median follow-up, 355 days). Only seven of 44 patients (16%) regained ovarian function. Of the 33 who received myeloablative regimens, six (18%) regained ovarian function. However, among the 11 who received nonmyeloablative regimens, only one (9%) regained ovarian function (p ‫؍‬ .66).Conclusion. Leuprolide did not preserve ovarian function in patients who underwent HSCT using either myeloablative or nonmyeloablative regimens. Other measures that protect ovarian function need to be investigated. The Oncologist 2012;17:233-238

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A 35-mo-old spayed female mixed-breed cat with continuous vomiting, emaciation, and abdominal distention for 2 wk was presented to a private veterinary clinic for evaluation. At 71 d after the initial visit, the cat died with anemia, jaundice, and hypoalbuminemia, and was subjected to autopsy. Grossly, numerous firm masses, 0.5-2.5 cm diameter, were randomly located in the left lobe of the pancreas. Histologic examination revealed that the pancreatic mass consisted of 2 tumor cell types: mostly small round cells with a minority of epithelial cells. The small cells were arranged in nests of various sizes, which were separated by thin fibrous stroma, and had small, round, hyperchromatic nuclei, scant cytoplasm containing argyrophilic granules, and often formed rosettes. The epithelial cells formed luminal structures. Metastases were observed in the liver, greater omentum, and pancreatic, gastric, pulmonary, and mediastinal lymph nodes. Immunohistochemical examination revealed that the small cells were positive for vimentin, neuron-specific enolase, chromogranin A, cytokeratin (CK) AE1/AE3, and trypsin, whereas the epithelial cells were positive for AE1/AE3, trypsin, CK19, and nestin. Ultrastructurally, the small cells contained abundant electron-dense granules, ~200 nm diameter, whereas the epithelial cells had apical microvilli and numerous zymogen granules, ~300 nm diameter. These findings indicated that the tumor was a pancreatic neuroendocrine carcinoma with exocrine differentiation and systemic metastases.

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Large numbers of genes are responsible for Leigh syndrome (LS), making genetic confirmation of LS difficult. We screened our patients with LS using a limited set of 21 primers encompassing the frequently reported gene for the respiratory chain complexes I (ND1–ND6, and ND4L), IV(SURF1), and V(ATP6) and the pyruvate dehydrogenase E1α-subunit. Of 18 LS patients, we identified mutations in 11 patients, including 7 in mDNA (two with ATP6), 4 in nuclear (three with SURF1). Overall, we identified mutations in 61% of LS patients (11/18 individuals) in this cohort. Sanger sequencing with our limited set of primers allowed us a rapid genetic confirmation of more than half of the LS patients and it appears to be efficient as a primary genetic screening in this cohort.

ABSTRACT:We carried out the CS-30 (30 second sitting to standing) test on 60 elderly subjects classified as care group 1 or group 2 based on the elderly care grading system. Subjects did not have any difficulty in toileting and had no conditions such as dementia or central nervous system diseases. The relationship between stand up ability and excretion independence was examined. Subjects who were both able and unable to safely and independently use toilets within a facility were divided into an excretion independent group and an excretion independent difficulty group. Each group then carried out the Japanese CS-30 test using the Jones method. The excretion independent difficulty group showed a significant decline in the CS-30 test (p<0.01) when compared to the excretion in dependent group. Discriminant characteristic analysis indicated a possible distinction between both groups at a cut-point of 5.5 stand ups (discriminant rate 94.4%, sensitivity 85.0%). However, careful consideration should be given to putting these results to practical use at home due to environmental differences in individual households.

A 69-year-old man with prostatic cancer under palliative care developed isolated right-sided oculomotor nerve palsy with pupillary impairment and persistent ocular pain. Cranial magnetic resonance imaging demonstrated metastasis of prostatic cancer to the right-sided cavernous sinus and orbital apex. In the English language literature, there are only six reported cases of isolated oculomotor nerve palsy secondary to prostatic cancer. In all cases, although there was metastatic lesion in the vicinity of the cavernous sinus, ocular pain did not develop. In the current patient, because metastatic tumour might involve the right-sided oculomotor nerve as well as lacrimal nerve, ocular pain developed. ARTICLE HISTORY