Acute Disease ; Adult ; Glomerulonephritis ; etiology ; Hepatitis ; etiology ; Humans ; Male ; Meningitis, Aseptic ; etiology ; Pancreatitis ; etiology ; Typhoid Fever ; complications

Aortic Coarctation ; diagnosis ; Female ; Humans ; Middle Aged ; Paraparesis ; diagnosis

Acute Disease ; Arthritis ; diagnosis ; Edema ; diagnosis ; Female ; Humans ; Middle Aged ; Skin Diseases ; diagnosis ; Syndrome ; Synovitis ; diagnosis

Solitary metastases from colorectal carcinoma in the absence of hepatic or pulmonary metastases are rare. These can have a diverse imaging appearance, particularly after chemotherapy. It is important identify patients with solitary skeletal metastases, as they have a better prognosis than those with multiple skeletal or visceral metastases. We describe an unusual case of a solitary metastasis to the femur in a case of colon carcinoma that went undiagnosed and later presented with imaging features of osteogenic sarcoma.
Adult ; Bone Neoplasms/diagnosis/radiography/secondary ; Carcinoma/*diagnosis/pathology/radiography ; Colorectal Neoplasms/*diagnosis/pathology/radiography ; Female ; Femur/radiography ; Humans ; Magnetic Resonance Imaging ; Prognosis ; Tomography, X-Ray Computed

Background: Amenorrhea is the absence of menstrual periods. It has multiple social consequences as it may leads to infertility. This case control study was conducted for determining the association of thyroid hormones with hyperprolactinemia in patient with amenorrhea. Methods: We investigated 50 women with diagnosed cases of secondary amenorrhoea, who attended UCMS hospital, for hormonal evaluations. Fifty two healthy women were taken as the controls. The thyroid dysfunction and serum prolactin level were reviewed in cases and in the controls. Results: Mean serum prolactin level was found to be significantly higher in the cases as compared to the controls. Mean serum fT3 and fT4 level in the hyperprolactinemic cases (mean = 2.67, SD = 1.04 pg/ml) and (mean = 1.38, SD = 0.51 ng/dl respectively) were slightly lower as compared to normoprolactinemic cases (mean = 3.21, SD = 1.86 pg/ml) and (mean = 1.73, SD = 1.37 ng/dl) respectively. Mean TSH of normoprolactinemic and hyperprolactinemic cases were comparable (P = 0.049). There was positive correlation between prolactin, BMI and TSH whereas negative correlation of prolactin was seen with fT3, fT4 and age. In hyperprolactainemic cases, prolactin was found to be negatively correlated with TSH (r = -0.155, P = 0.491) whereas prolactin was positively correlated with TSH (r = 0.296, P = 0.126) in normoprolactainemic cases. Conclusions: Thus, hyperprolactinemia with thyroid dysfunction may be contributory hormonal factor in patient with amenorrhoea and as such, estimation of prolactin, fT3, fT4 and TSH should be included for diagnostic evaluation of amenorrhea.

Breast carcinoma is a heterogeneous disease that has exhibited rapid resistance to treatment in the last decade. Depending genotype and phenotype of breast cancer, there are discernible differences in DNA repair protein responses including DNA double strand break repair. It is a fact that different molecular sub-types of breast carcinoma activate these dedicated protein pathways in a distinct manner. The DNA double-strand damage repair machinery is manipulated by breast carcinoma to selectively repair the damage or insults inflicted by the genotoxic effects of chemotherapy or radiation therapy. The two DNA double-strand break repair pathways employed by breast carcinoma are homologous recombination and non-homologous end joining. In recent decades, therapeutic interventions targeting one or more factors involved in repairing DNA double-strand breaks inflicted by chemo/radiation therapy have been widely studied. Herein, this review paper summarizes the recent evidence and ongoing clinical trials citing potential therapeutic combinatorial interventions targeting DNA double-strand break repair pathways in breast carcinoma.
Breast Neoplasms* ; Breast* ; DNA Repair ; DNA* ; Drug Therapy ; Genotype ; Homologous Recombination ; Phenotype ; Radiotherapy

Among the genotoxic drug regimens, doxorubicin (DOX) is known for its high-dose side effects in several carcinomas, including cervical cancer. This study reports on testing the combined use of a DOX genotoxic drug and SCR-7 non-homologous end joining (NHEJ) inhibitor for HeLa cells. An in vitro DNA damaging assay of DOX was performed on plasmid and genomic DNA substrate. In vitro cytotoxicity was investigated using trypan blue dye exclusion, DNA metabolizing, and propidium iodide-based flow cytometric assays. DOX (between 20–100 μM) displayed clear DNA binding and interaction, such as the shearing and smearing of plasmid and genomic DNA. DNA metabolizing assay data indicate that HeLa lysate with DOX and SCR-7 treatment exhibited better in vitro plasmid DNA stability compared with DOX treatment alone. SCR-7 augmented the effects of low-dose DOX by demonstrating enhanced cell death from 15% to 50%. The flow cytometric data also supported that the combination of SCR-7 with DOX lead to a 23% increase in propidium iodide-based HeLa staining, thus indicating enhanced death. In summary, the inhibition of NHEJ DNA repair pathway can potentiate low-dose DOX to produce appreciable cytotoxicity in HeLa cells.
Cell Death ; DNA ; DNA Damage ; DNA End-Joining Repair ; DNA Repair ; Doxorubicin* ; Drug Therapy ; Genomic Instability ; HeLa Cells* ; Humans ; In Vitro Techniques ; Plasmids ; Propidium ; Trypan Blue ; Uterine Cervical Neoplasms

Several genetic and epigenetic theories have been suggested to explain the intricacies of life and death. However, several questions remain unsettled regarding cellular death events, particularly of living tissue in the case of cancer patients, such as the fate and adaptation of cancer cells after biological death. It is possible that cancer cells can display the intent to communicate with the external environment after biological death by means of molecular, genetic, and epigenetic pathways. Whether these cancer cells contain special information in the form of coding that may help them survive beyond the biological death of cancer patients is unknown. To understand these queries in the cancer field, we hypothesize the epigenomic hard drive (EHD) as a cellular component to record and store global epigenetic events in cancerous and non-cancerous tissues of cancer patients. This mini-review presents the novel concept of EHD that is reinforced with the existing knowledge of genetic and epigenetic events in cancer. Further, we summarize the EHD understanding that may impart much potential and interest for basic and clinical scientists to unravel mechanisms of carcinogenesis, therapeutic markers, and differential drug responses.
Carcinogenesis ; Chromatin ; Clinical Coding ; Epigenomics* ; Humans