Substituting Resistance Spot Welding with Flexible Laser Spot Welding to Join Ultra-Thin Foil of Inconel 718 to Thick 410 Steel

This paper investigated various aspects of replacing existing micro-resistance spot welding (micro-RSW) with micro-laser spot welding for joining Inconel 718 thin foils to thick 410 steel stack-up to allow faster, non-contact joining together with flexibility in spot positioning and removal of tip dressing required for RSW electrodes. The joint quality was evaluated based on the mechanical strength, microstructural characteristics and joint strength at elevated temperature as these joints are often used for high-temperature applications. Experimental investigations were performed using micro-RSW and micro-laser spot welding to obtain the 90° peel and lap shear specimens, each comprising four spots. The obtained strength from laser joints was significantly higher than that of micro-RSW joints due to larger weld nugget formation and interface width. The process map for obtaining good quality welds was also identified, and about a 17% reduction in joint strength was obtained when welded specimens were subjected to elevated temperature (i.e., 500 °C) in comparison with room temperature. This reduction was compensated for using the flexibility of laser welding to add two extra spots. The overall performance of the micro-laser spot welds was found to be better than the micro-RSW considering joint strength, flexibility in placing the spots and time to produce the welds.     

Reduced Port Laparoscopic Cholecystectomy: Single and a Half Incision Lap Chole

Laparoscopic cholecystectomy has almost replaced the age-old procedure of open cholecystectomy for gall stone disease. Further attempts are made to reduce the number of ports to give maximum benefits of minimally invasive surgery. The author has developed a technique where 10-mm port in supraumbilical area and 5-mm port in epigastric area are used and hence the nomenclature of single and a half incision laparoscopic cholecystectomy. It is different from two-port laparoscopic cholecystectomy where the second port is 10 mm. In total, 69 cases are performed without any complication. Conclusion: In our technique of single and a half incision laparoscopic cholecystectomy patients’ safety is as much as in a conventional four-port surgery. Surgeon is comfortable to perform this operation. Cosmetically, it is better than four-port laparoscopic cholecystectomy without increase in cost. So, in our opinion, our technique should be acceptable to all surgeons and can give benefits of minimal access surgery to masses of people.     

Molecular Motions in Sucrose-PVP and Sucrose-Sorbitol Dispersions—II. Implications of Annealing on Secondary Relaxations

Purpose

To determine the effect of annealing on the two secondary relaxations in amorphous sucrose and in sucrose solid dispersions.

Methods

Sucrose was co-lyophilized with either PVP or sorbitol, annealed for different time periods and analyzed by dielectric spectroscopy.

Results

In an earlier investigation, we had documented the effect of PVP and sorbitol on the primary and the two secondary relaxations in amorphous sucrose solid dispersions (1). Here we investigated the effect of annealing on local motions, both in amorphous sucrose and in the dispersions. The average relaxation time of the local motion (irrespective of origin) in sucrose, decreased upon annealing. However, the heterogeneity in relaxation time distribution as well as the dielectric strength decreased only for β₁- (the slower relaxation) but not for β₂-relaxations. The effect of annealing on β₂-relaxation times was neutralized by sorbitol while PVP negated the effect of annealing on both β₁- and β₂-relaxations.

Conclusions

An increase in local mobility of sucrose brought about by annealing could be negated with an additive.     

AKR Murine Leukemia Virus Genome: Frequency of Sequences in DNA of High-, Low-, and Non-Virus-Yielding Mouse Strains

Studies with a single-stranded DNA probe complementary to the RNA of mouse-tropic AKR murine leukemia virus indicate that the complete genome of the AKR-type murine leukemia virus is present in the DNA of high- and low-virus-yielding mouse strains, while DNA of non-virus-yielding strains contains only a part of the genome. Furthermore, in those strains where the genome is complete, two populations of virus-specific DNA sequences can be identified (more abundant and less abundant species) according to their rate of association with the probe. Low-virus-yielding mouse strains contain fewer copies of the less abundant species and, consequently, fewer complete viral genomes than do high-virus-yielding strains. Thus, in the ten strains tested, there is a good correlation between completeness of the genome of AKR-type murine leukemia virus in cellular DNA and the capacity of the cells to release infectious AKR-type murine leukemia virus. Moreover, the number of complete viral genomes correlates with the frequency of infectious virus production by virus-positive strains. DNA from wild Mus musculus also contained viral sequences, the sample tested showing reassociation kinetics identical to the non-virus-producing strains.     

Central nervous system infection in a murine retrovirus-induced immunodeficiency syndrome

Astrocyte-enriched primary glial cultures (AGC) from C57BL/6 mice were found to be highly susceptible to infection with the replication competent components of LP-BM5, consisting of the ecotropic and mink cell focus-inducing (MCF) helper murine leukemia viruses (MuLVs). The presence in infected AGC of defective LP-BM5 MuLV genome, a critical component for induction of the disease referred to as murine AIDS, was confirmed by Southern blot hybridization using a probe reactive with the p12 gag sequence of the 4.9 kb defective genome. Electron microscopic studies demonstrated C-type retrovirus particles in both astrocytes and microglial cells. In vivo studies demonstrated that the ecotropic MuLVs and the defective genome could be detected within AGC obtained form either 14-day-old mice following intraperitoneal inoculation or 7-day-old mice following intracranial inoculation. These findings suggest that: (1) the central nervous system (CNS) infection is present at an early stage in murine AIDS, (2) both astrocytes and microglial cells are possible CNS targets in which helper MuLVs replicate, and (3) these cells can harbor the defective genome that is a critical component for disease induction.     

Altered protein expressions in chronic PCB-153-induced human liver (HepG2) cells

Polychlorinated biphenyls (PCBs) are a group of persistent and widely distributed environmental pollutants that have various deleterious effects, e.g., neurotoxic, endocrine disruption and reproductive abnormalities, including cancers. Chronic exposure to environmentally hazardous chemicals like PCBs is of great concern to human health. It has been reported earlier that apoptotic proteins change in rats under chronic PCB treatment. It is of importance to determine if chronically exposed human cells develop a different protein expression. In the present study, the authors chronically exposed metabolically competent human liver (HepG2) cells at 50 to 100 microM to examine the role of the well-known environmentally hazardous pollutant non-coplanar 2,2',4,4',5,5'-hexachlorobiphenyl (PCB-153) to study cell death. After 12 weeks of exposure these cells showed significant changes in apoptotic death in subsequent trypan blue growth assay, fluorescence microscopy, DNA fragmentation, and immunoblotting studies. Interestingly, chronically exposed cells showed marked differences in apoptotic and/or death-related proteins (e.g., Bcl2, Bak, and the pro and active forms of caspase-9, which were up-regulated), in contrast to acutely exposed (i.e., 48-h PCB-153 exposed) cells, which maintained linear growth despite repeated exposures. Similarly, tumor suppressor protein p53, proto-oncogene c-myc, and cell cycle regulator protein p21 were also up-regulated compared to nonchronically exposed HepG2 Cells. The results indicated that PCB-153-induced chronic exposure significantly altered different apoptotic (e.g., Bcl2, Bak, caspase-3) and tumor suppressor (e.g., p21, p53, and c-myc) proteins in the cellular model. These results suggest that chronic exposure to PCB-153 can induce cell survival by altering several apoptotic and tumor suppressor proteins.