Enigma of scapular foramen and tunnels: an untold story.

PURPOSE: The study was undertaken to make a qualitative and quantitative assessment of unnamed foramen and tunnels in adult human scapulae with aid of plain and contrast radiographs. MATERIALS AND METHODS: A total of 120 dry bones, 60 each of the right and the left side were included in the study. Distribution of these foramina and tunnels was noted for their number, side, location, course and communication. Their morphometry was done using Vernier's caliper. RESULTS: Incidence of scapular foramina was 7.5% (R > L), whereas scapular tunnels were seen in 15.8% cases. Incidence of the sinuous, curved, and straight tunnels was found to be 50, 39, and 10.7% respectively. Left-sided tunnels were longer than the right ones. Plain and contrast radiographs were taken to confirm the findings. CONCLUSION: Anatomy literature describes only two scapular foramina, namely, nutrient foramen and suprascapular foramen/notch in a great zeal; occurrence of such anonymous foramina is hardly discussed. Through this study, there is an endeavor towards unfolding the mystery of scapular foramina in terms of their morphometry and distribution, the knowledge of which will aid clinicians, forensic experts, and surgeons in better diagnosis and management of clinical cases.

Gender Linked Metric Analysis of Portal Vein: A Sonographic Appraisal.

INTRODUCTION: Portal hypertension is one of the most mystifying and disconcerting abdominal ailment. Ultrasonography (USG) is an effective diagnostic tool for its prompt management. Knowledge of normal calibre of portal vein in a local setting is essential as literature reports contrasting values in different regions. It helps in early diagnosis of portal hypertension even before it is clinically manifested thereby assisting clinicians and interventional radiologists in pertinent management. AIM: Study was aimed to evaluate the Portal Vein Diameter (PVD) and find its correlation with gender by using USG in North Indian population. MATERIALS AND METHODS: A total of 300 healthy adults were included in the study. Portal vein diameter was measured in supine position and normal respiration by grey scale USG. The portal vein diameter was correlated with age and gender statistically using independent Student's t-test and ANOVA. RESULTS: Mean PVD of (9.49±1.03 mm) was observed in the present cross-sectional study. Male showed a significantly higher mean PVD (9.70±1.02 mm) as compared to females (9.10±0.94 mm). CONCLUSION: Scarcity of information concerning ultrasonographically measured standard portal vein diameter and inconstant values reported in literature necessitates the need for establishing local standard value. In the given subset of population the portal vein diameter was influenced by the gender. The information will be helpful in prompt diagnosis and management of portal hypertension.

Absence of Posterior Triangle: Clinical and Embryological Perspective.

Sternocleidomastoid (SCM) and Trapezius (TM) muscle present in the cervical region serves as an important landmark in forming boundaries of posterior triangle of neck. This case reports a continuous muscle sheet obscuring the left posterior triangle in the neck of a 60-year-old Indian male cadaver. An unfamiliar oval gap was observed in its posterosuperior portion. Description of such a variant in anatomical literature is rare and is scarcely reported. An attempt has been made to portray its embryological and phylogenetic basis. In addition authors have endeavoured to discuss its clinical implications. Awareness of such anatomical variations is relevant for the operating surgeons in their endeavour to perform various reconstruction surgeries of head and neck, radiologists while concluding various levels in Computed Tomography (CT) and Magnetic Resonance Images (MRI) of the region and to the anaesthetists in their search for nerves and vessels while attempting various anaesthetic procedures.

Cisplatin primes murine peritoneal macrophages for enhanced expression of nitric oxide, proinflammatory cytokines, TLRs, transcription factors and activation of MAP kinases upon co-incubation with L929 cells.

Cisplatin, a chemotherapeutic drug, may also act as a biological response modifier. Cisplatin (10mug/ml) treatment of macrophages for 24h activates them to produce enhanced amounts of nitric oxide (NO), ROI, proinflammatory cytokines and exhibit increased tumoricidal activity, which may or may not be contact mediated. In the present investigation, we report that the treatment of macrophages with cisplatin for a short period of 2h is sufficient to make them more receptive to interaction with tumor cells. Macrophages pretreated with cisplatin for 2h, and co-incubated with L929 cells, produced enhanced NO, TNF-alpha, IL-1beta, IL-12 and IFN-gamma. Production of NO, TNF-alpha, IL-1beta, IL-12 and IFN-gamma was maximum at 24h of co-incubation. Enhanced transcription of iNOS, TNF-alpha, IL-1beta, IL-12 and IFN-gamma genes in cisplatin-pretreated macrophages were observed between 12 and 24h of co-incubation with L929 cells. Cisplatin-treated macrophages on co-incubation with L929 cells also expressed enhanced transcription of Toll-like receptor (TLR)-2 and TLR-4 genes and their proteins. It is observed that cisplatin-pretreated macrophages on co-incubation with L929 cells showed activation of mitogen-activated protein (MAP) kinases and NF-kappaB. Pharmacological inhibitors like PD98059, SB202190 and wortmannin strongly inhibited the production of NO and proinflammatory cytokines suggesting the probable role of p42/44, p38 MAPK and PI3K in the above process. The c-Jun amino terminal kinase (JNK) inhibitor SP600125 was less effective in inhibiting the production of NO and proinflammatory cytokines. The data thus suggests that pretreatment of macrophages with cisplatin makes them biologically more responsive to interaction with L929 cells and become activated.

Differential expression of Toll-like receptors in murine peritoneal macrophages in vitro on treatment with cisplatin.

In the present study, we have investigated the differential expression of Toll-like receptors [(TLRs) 1-9] in murine peritoneal macrophages in vitro, on treatment with cis-diaminedichloroplatinum (II) (cisplatin). It is demonstrated that cisplatin induces the expression of TLRs and is a potent activator of Toll-signaling pathway. The enhanced expression of TLR2, -3, -4, -5, -6, -7, -8 and -9 is observed at different time intervals after 5 microg ml(-1) cisplatin treatment. The expression of downstream signaling molecules of TLR-signaling pathway--myeloid differentiation factor 88, IRAK1, tumor necrosis factor receptor-associated factor 6 and transcription factors IRF3 and nuclear factor-kappaB (NF-kappaB)--has also been investigated. The expression of TLR2, -3, -4 and -9 was down-regulated in cisplatin-treated macrophages in the presence of inhibitors of mitogen-activated protein kinases and NF-kappaB pathways, suggesting a role of these pathways in cisplatin-induced TLR expression. It is also observed that pre-treatment of macrophages with cisplatin and subsequent incubation with TLR ligands significantly enhanced the production of pro-inflammatory cytokines (tumor necrosis factor-alpha, IFN-gamma, IL-1beta and IL-12) and iNOS expression in macrophages. The data suggest that treatment of macrophages with cisplatin renders them more susceptible to subsequent induction of pro-inflammatory cytokines and iNOS expression by different TLR ligands. It is proposed that the pharmacological reagents like cisplatin can be used to manipulate the innate immune responses, which may be effectively used for the development of novel therapeutic approaches.

Cisplatin-treated murine peritoneal macrophages induce apoptosis in L929 cells: role of Fas-Fas ligand and tumor necrosis factor-tumor necrosis factor receptor 1.

Cisplatin [cis-diamminedichloroplatinum (II)]-treated murine peritoneal macrophages interact with L929 cells in vitro in a sequential manner, resulting in the formation of contact between the two cells. This interaction leads to the death of L929 cells by the process of apoptosis. The detailed investigations have suggested the involvement of two different pathways in macrophage-mediated L929 cell apoptosis. It is observed that the induction of apoptosis in L929 cells by cisplatin-treated macrophages is contact dependent and is mediated through Fas-Fas ligand and tumor necrosis factor-tumor necrosis factor receptor 1 pathways. This conclusion was based on the Western blot and immunoprecipitation analysis of Fas-Fas ligand, tumor necrosis factor-tumor necrosis factor receptor 1, Fas-associated death domain and tumor necrosis factor receptor-associated death domain. The Fas-Fas ligand interaction between macrophages and L929 cells increased the expression of Fas-associated death domain, and tumor necrosis factor-tumor necrosis factor receptor 1 interaction between macrophages and L929 cells increased the expression of tumor necrosis factor receptor-associated death domain in L929 cells. The induction of apoptosis in L929 cells was investigated by DNA fragmentation, Annexin V staining and Western blot analysis of Bax, Bcl-2, Bid, cytochrome c, poly(ADP ribose) polymerase, CAD, caspase-8 and caspase-3.

Interaction between cisplatin treated murine peritoneal macrophages and L929 cells: involvement of adhesion molecules, cytoskeletons, upregulation of Ca2+ and nitric oxide dependent cytotoxicity.

Murine peritoneal macrophages on treatment with cisplatin (10 microg/ml) showed increased binding to L929 cells. Cisplatin treated macrophage on co-incubation with L929 cells form a distinct cytoplasmic contact between the two cells. The plasmalemmae of the two cells fuse over a large surface area. The formation of contact between the cisplatin treated macrophage and L929 cell results in the induction of apoptosis in L929 cell. Untreated macrophages did not form a contact with L929 cells and no apoptosis is observed in L929 cells. Immunofluorescence microscopical studies clearly show the participation of cytoskeleton and the adhesion molecules in the formation of contact between the two cells. Further, a significant enhancement of the expression of iNOS and cytosolic Ca2+ was observed in cisplatin treated macrophages co-incubated with L929 cells. Cisplatin treated macrophages produced significant amount of NO when co-incubated with L929 cells, while there was minimal production of NO by untreated macrophages co-incubated with L929 cells. Cisplatin treated macrophage-induced L929 cell death was NO dependent, since L-NMMA (500 microM) significantly inhibited the cytotoxicity of L929 cells. The addition of excess L-arginine (2mM) reversed the L-NMMA induced inhibition of NO production and L929 cell cytotoxicity.