A massive rock and ice avalanche caused the 2021 disaster at Chamoli, Indian Himalaya.

On 7 February 2021, a catastrophic mass flow descended the Ronti Gad, Rishiganga, and Dhauliganga valleys in Chamoli, Uttarakhand, India, causing widespread devastation and severely damaging two hydropower projects. More than 200 people were killed or are missing. Our analysis of satellite imagery, seismic records, numerical model results, and eyewitness videos reveals that ~27 × 106 cubic meters of rock and glacier ice collapsed from the steep north face of Ronti Peak. The rock and ice avalanche rapidly transformed into an extraordinarily large and mobile debris flow that transported boulders greater than 20 meters in diameter and scoured the valley walls up to 220 meters above the valley floor. The intersection of the hazard cascade with downvalley infrastructure resulted in a disaster, which highlights key questions about adequate monitoring and sustainable development in the Himalaya as well as other remote, high-mountain environments.

The effect of amount of crude oil on extent of its biodegradation in open water- and sandy beach-laboratory simulations.

We examined the biodegradation of varying amounts of artificially weathered Alaskan North Slope crude oil in laboratory microcosm test systems that use natural seawater and simulate spills in open water and on sandy beaches. The model bioremediation treatment consisted of periodic applications of marine bacteria, selected to degrade n-alkanes and a range of aromatic compounds, suspended in a salts solution that supplied inorganic nitrogen and phosphorous. Beach microcosms dosed with low and high oiling lost an average of 22.5% and 11.3% oil weight, respectively. Open-water microcosms dosed with high and low oiling lost 19.1% and 2.9% oil weight, respectively. Thus, the lower doses of oil were more efficiently degraded. The model bioremediation treatment also affected a greater number of selected analytical endpoints in the lower-oil-dose than higher-dose experiments and the former showed more substantial degradation of recalcitrant components. Above a certain threshold oil concentration, bioremediation did not effectively remove oil. Below this threshold the distinction between active bioremediation treatment and intrinsic biodegradation of the controls was less prominent; i.e., fewer of the oil components were statistically depleted by remediation treatment relative to controls. Furthermore, the oil-dose range over which bioremediation was realized in these systems occurred at very low oiling levels. Thus, under the environmental conditions simulated in these microcosms, the effectiveness of bioremediation peaked over a rather narrow low-dose oiling range.

Analysis of the CC chemokine receptor 3 gene reveals a complex 5' exon organization, a functional role for untranslated exon 1, and a broadly active promoter with eosinophil-selective elements.

To understand the regulation of CC chemokine receptor 3 (CCR3) expression, its gene structure and promoter have been characterized. The CCR3 gene contains 4 exons that give rise to multiple messenger RNA (mRNA) species by alternative splicing. Exon 1 is present in all transcripts, whereas exon 2 or 3 is present at low frequency (< 10%). Exon 4 contains the open reading frame and 11 bp of the 5' untranslated region. Northern analysis revealed 4 species of CCR3 mRNA. Direct sequencing revealed that the first 1 kb of the promoter and exon 1 contained only one mutation in 19 individuals, indicating that the CCR3 promoter and exon 1 are conserved between individuals. The first 1.6 kb of the 5' flanking region of exon 1 contained promoter elements including a TATA box and motifs for myeloid transcription factors and had strong promoter activity in eosinophilic, lymphoid, myeloid, and respiratory epithelial cell lines. Deletion analysis revealed differential regulation of the CCR3 promoter in eosinophilic and epithelial cells suggesting the presence of lineage-specific elements. Interestingly, exon 1 enhanced the activity of the promoter and this effect was especially prominent in eosinophilic cells. Thus, the human CCR3 gene has a complex 5' exon structure, a conserved promoter with strong activity in multiple cell types, and a functional 5' untranslated exon.

Sex hormones modulate the response of pulmonary perivascular inflammation to cyclophosphamide therapy in MRL/MpJ-lpr/lpr mice.

Responses of pulmonary perivascular infiltrates to immunosuppressive therapy with cyclophosphamide (CY) were evaluated in the MRL/MpJ-lpr/lpr (MRL/1) mouse, a model for the study of systemic lupus erythematosus. Male and female mice were divided into the following groups: controls injected with saline; intact mice receiving CY; castrated CY-treated mice; castrated, hormone implanted, CY-treated mice. CY treatment began at 30 days of age and animals were killed at 60 days of age. Lungs were fixed-inflated to 26 cm H2O pressure with glutaraldehyde-formaldehyde fixative. The pulmonary perivascular response to immunosuppressive therapy was graded depending on the extent of infiltrates surrounding 15 pulmonary vessels per animal. Intact males treated with CY alone had almost complete clearing of perivascular infiltrates, whereas intact females did not respond to therapy. Castrated CY-treated males showed a decreased response to CY compared to intact CY-treated males. Castrated, estradiol-implanted males had no response to CY therapy. Estradiol interfered with the therapeutic response to CY in male MRL/1 mice.

Pulmonary inflammation in autoimmune MRL/Mp-lpr/lpr mice. Histopathology and bronchoalveolar lavage evaluation.

Early detection of lupus pneumonitis is difficult because it requires lung biopsy. The authors describe here in detail the age-related histologic changes in pulmonary inflammation, the age-related changes in bronchoalveolar lavage (BAL), and the effect of cyclophosphamide (8 mg/kg) on pulmonary inflammation and bronchoalveolar lavage in MRL/Mp-lpr/lpr mouse, an animal model of systemic lupus erythematosus. To assess the evolution of pulmonary inflammation and response to cyclophosphamide therapy, they compared the age-related progression of pulmonary inflammation with sequential changes in BAL cell populations in this autoimmune mouse model. A striking similarity was noted between age-related changes in pulmonary inflammation and lymphocyte counts in BAL. A trend to reduction in histologic evidence of inflammation was reflected by lymphocytes in BAL in cyclophosphamide-treated (8 mg/kg/day) males but not in females. There was a striking sex-related difference in that the histologic evidence of pulmonary inflammation and bronchoalveolar lavage lymphocyte count in cyclophosphamide-treated males was significantly lower than cyclophosphamide-treated females of the same age.