Isolation of Stomatococcus mucilaginosus from drug user with endocarditis.

Stomatococcus mucilaginosus was isolated from the blood of a patient with endocarditis and a past history of drug abuse and aortic valve replacement. At autopsy, Gram stain of the aortic valve revealed gram-positive cocci. Our isolate was atypical for S. mucilaginosus in that colonies were nonmucoid and nonadherent to agar surfaces. Cellular capsules were demonstrated by light and electron microscopy. Phenotypic characteristics identified by conventional methods as well as profile numbers obtained by using two commercial identification systems for staphylococci, the API Staph-Ident and the dms Staph Trac, are presented. Practical tests that differentiate S. mucilaginosus from the genera Micrococcus and Staphylococcus include growth on nutrient agar containing salt and lysostaphin susceptibility. Additional tests that helped differentiate our isolate from group D streptococci included hydrolysis of L-pyrrolidonyl-beta-naphthylamide and streptococcal serogrouping.     

Allergic fungal sinusitis— A clinico-pathological study

The co-existence of fungal elements in allergic nasal Polyposis, has given rise to a distinct clinical entity known as ‘Allergic fungal sinusitis ’ (AF’S). Many a time, these fungal elements may not be diagnosed pre-operatively by routine diagnostic nasal endoscopy or CT scan of paranasal sinuses, due to the florid presentation of nasal polyps, which usually obscure the underlying fungal pathology. The diagnosis is often made intra-operatively. The post-operative confirmation of AFS is by histopathology, fungal smear, fungal culture, allergic murin study and fungal specific IgE titres. We report a series often such cases done in our institution, which highlight that AFS should be considered as a differential diagnosis in Sinonasal Polyposis cases, for their effective management.     

Subselective embolisation in management of JNA

Role of Embolisation in preoperative management of Nasopharyngeal angiofibroma is well established in present day therapeutic modalities. An improvised technique i.e., subselective embolisation has been provided by Interventional radiologists to fortify the therapeutic results. This study compares the final outcome of seven cases, four of which were embolised pre operatively. Each case was dealt with varying surgical approaches.     

Enhancement of cisplatin sensitivity of cisplatin-resistant human cervical carcinoma cells by bryostatin 1.

PURPOSE: Bryostatin 1, a unique protein kinase C (PKC) activator, is already in the clinical trials. An understanding of complex regulation of PKC by bryostatin 1 is essential for effective use of bryostatin 1 in the clinic. We have previously shown that the ability of bryostatin 1 to enhance cisplatin sensitivity correlated with its ability to down-regulate PKCdelta in HeLa cells. We have investigated how bryostatin 1 influences PKCdelta regulation in cisplatin-resistant HeLa (HeLa/CP) cells, and if bryostatin 1 could be used to reverse cisplatin resistance. EXPERIMENTAL DESIGN: Phorbol 12,13-dibutyrate (PDBu), bryostatin 1, and small interfering RNA were used to manipulate PKC level/activation status. Cell death was monitored by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, Annexin V dye-binding assay, and analysis of hypodiploid peak in a flow cytometer. RESULTS: Bryostatin 1 elicited a biphasic concentration response on PKCdelta down-regulation and cisplatin-induced cell death in HeLa/CP cells; the maximum effect was achieved with 1 nmol/L bryostatin 1. Down-regulation of PKCalpha increased with increasing concentrations of bryostatin 1. PDBu induced down-regulation of PKCalpha in HeLa and HeLa/CP cells but it had little effect on PKCdelta down-regulation in HeLa/CP cells. However, both PDBu and bryostatin 1 enhanced the sensitivity of HeLa/CP cells to cisplatin. Knockdown of PKCdelta by small interfering RNA inhibited cisplatin-induced apoptosis but knockdown of PKCalpha enhanced cisplatin-induced cell death. CONCLUSIONS: These results suggest that although PKCdelta acts as a proapoptotic protein, full-length PKCdelta may inhibit cisplatin-induced cell death. Thus, persistent activation/down-regulation of PKCdelta by bryostatin 1 was associated with cisplatin sensitization. Furthermore, PKCalpha acts as an antiapoptotic protein and down-regulation of PKCalpha by PDBu was associated with cellular sensitization to cisplatin.     

Mitoxantrone, mitomycin-C, methotrexate combination chemotherapy with radiotherapy and/or surgery in stage III (T4B, NO-2, M0) breast cancer

Results of primary surgery with or without locoregional radiotherapy (LRRT) are poor in stage III (T4b, NO-2, M0) breast cancer. Combination of mitoxantrone, mitomycin-c and methotrexate (MMM) has been reported to be as efficacious as doxorubicin based protocols with advantages of reduced nausea, vomiting, alopecia and cardiotoxicity. We tested MMM chemotherapy with LRRT and surgery in locally advanced breast cancer (LABC) with a view to assess response, survival, breast conservation, cost and toxicity. Fifty two previously untreated patients were given Mitoxantrone: 8 mg/m sq by infusion on days 1 and 21, Mitomycin-C: 8 mg/m sq by infusion on day 1 and Methotrexate: 35 mg/m sq i.v. on days 1 and 21. Cycles were repeated every 42 days. After 3 cycles LRRT was given if lump reduced to less than 2 cms. Otherwise patients were subjected to modified radical mastectomy (MRM) or radical mastectomy (RM). Following this 3 more cycles of chemotherapy were given. Patients with soft tissue, skin or heavy nodal involvement also received LRRT. Tamoxifen 20 mg daily was prescribed at the end of chemotherapy to postmenopausal patients. Complete/partial responses were seen in 5 and 26 patients, respectively after chemotherapy giving an overall response of 59.5%. Twenty four patients each had LRRT and MRM/RM. Responses could be significantly enhanced by LRRT/and or surgery. Nineteen out of 25 relapses were at distant sites. Breast conservation was achieved in 24/52 (46%) patients. Three year disease free and overall survival was 54% and 65%, respectively. There was 1 toxic death. Severe prolonged myelosuppresion was seen in those who also received LRRT. Mucositis, alopecia, nausea and vomiting were minor problems. Overall, combination was less expensive than doxorubicin based protocols.     

Congenital methemoglobinemia due to NADH-methemoglobin reductase deficiency in three Indian families

Congenital methemoglobinemia is a relatively rare clinical disorder characterized by life-long cyanosis, caused by either an inherited mutant hemoglobin (Hb-M) or deficiency of physiologically active NADH-dependent methemoglobin reductase (NADH-MR). NADH-MR deficiency leads to two different types of recessive congenital methemoglobinemia. In type I, cyanosis is the only major symptom and NADH-MR deficiency is restricted only to the red blood cells. In type II, cyanosis is associated with severe mental retardation and neurological impairment. The objective of this study is to establish the cause of cyanosis in our cases of congenital methaemoglobinemia. Erythrocyte NADH-MR activity was assayed spectrophotometrically. Spectral analysis of the hemolysate treated with potassium ferricyanide was recorded between 400-700 nm and Hb electrophoresis on starch gel at pH 7.0 was done to rule out the presence of Hb-M. NADH-MR deficiency was detected in 3 families. There was a history of consanguinity in one of these cases. The three propositi presented with breathlessness, fever and peripheral cyanosis. There was no history of cardiac illness or exposure to drugs and chemicals. There were no signs and symptoms of mental retardation. The presence of Hb-M was ruled out. Hb-A2, Hb-F, G6PD activity and reduced glutathione levels were normal. NADH-MR activity in all the cases ranged from 4.1 to 9.2 IU/g Hb (normal range 7.0-24.0 IU/g Hb). We describe NADH-MR deficiency in three unrelated cases (age 4 months to 6 years) where the activity of the enzyme was 30-40% of normal. These three cases of congenital methemoglobinemia are due to type-I NADH-MR deficiency without mental retardation.     

New observations on carrying angle

Based on experiments on fresh cadaveric and accidentally amputated 8 upper limbs of children, study of ulnae for presence and absence of non articular strip on the trochlear notch, measurements of carrying angle, length of forearm bones, pronation-supination, height and weight in 2250 infants, children and adults of various age groups and clinical observations on 800 cases of injuries around elbow many new facts have been observed about the development of the carrying angle and its significance in the etiopathogenesis of various types of fractures seen around the elbow. The carrying angle develops in response to pronation of the forearm and is dependent on length of the forearm bones. Lesser the length of forearm bones greater is the carrying angle. So the carrying angle is more in shorter persons as compared to taller persons. It is abduction at the shoulder and not the carrying angle which keeps the swinging upper limbs away from the side of the pelvis during walking. Carrying angle is not a secondary sex character. The type of fracture a child sustains after fall on outstretched hand is also determined by the value of the carrying angle. A new type of fracture hitherto undescribed in the literature, T-Y fracture of the distal humeral epiphysis is also reported.