Cold exposure is a major physiological stimulus that promotes adipose tissue browning and enhances thermogenic capacity. As a cold-tolerant breed, Min pigs may rely on distinct adaptive mechanisms in adipose tissues, but how different adipose depots respond to cold stress remains unclear. This study systematically examines how cold exposure affects adipose tissue morphology, thermogenic gene expression, and the differentiation potential of preadipocytes derived from four adipose depots-cervical, axillary, perirenal, and inguinal-in Min pigs. Adipose tissues from the four depots were collected and analyzed using infrared thermography, histological staining, scanning electron microscopy, real-time quantitative PCR, Western blotting and in vitro differentiation assays. The results demonstrated that cold stress induced depot-specific remodeling patterns. Infrared thermography showed that the subcutaneous adipose depots including inguinal and axillary depots maintained relatively higher surface temperatures following cold exposure. Histological and ultrastructural analyses revealed typical beige-like characteristics in inguinal depots, including the accumulation of small lipid droplets, whereas changes in other depots were minimal. Molecular analyses further confirmed this heterogeneity: inguinal depots exhibited the strongest beiging response, characterized by significant upregulation of key thermogenic markers (PGC1α, UCP3, and DIO2) and lipolytic genes (HSL and ATGL) at the mRNA and/or protein levels. In contrast, visceral adipose depots showed weak or suppressed thermogenic activation. In vitro differentiation assays demonstrated that preadipocytes isolated from inguinal depot had the strongest beiging potential, forming tightly packed small lipid droplets and markedly increasing the expression of beige adipose-related genes upon induction. In conclusion, this study demonstrates that cold stress induces distinct beige remodeling across adipose depots in Min pigs, with the inguinal depot exhibiting the strongest thermogenic response and differentiation potential at morphological, molecular, and cellular levels. These findings identify the inguinal depot as a key site for adaptive thermogenesis and provide novel insights into adipose tissue remodeling and environmental adaptation in large mammals.

Branching is a key determinant of plant architecture, directly influencing growth, yield, and resource allocation. High temperature (HT) inhibits plant growth and development, often leading to alterations in plant architecture. However, the molecular mechanisms underlying temperature-induced inhibition of branching remain elusive. Here, we discovered that CmBRC1a is strongly induced by HT and inhibits axillary bud development in chrysanthemum. We further demonstrated that the heat shock transcription factor CmHSFA3 directly activates CmBRC1a by binding to its promoter, thus acting as its upstream regulator. Overexpression of CmHSFA3 further confirmed its role in suppressing branching. The finding that HT cannot completely suppress the enhanced branching phenotype of CmBRC1a knockdown lines suggests that HT-regulated branching is not entirely dependent on CmBRC1a. Similar to previously reported BRC1-mediated pathways, CmBRC1a directly activates the expression of CmHB40, thereby increasing abscisic acid (ABA) accumulation, which ultimately inhibits shoot branching. Our findings reveal CmHSFA3-CmBRC1a-CmHB40 module inhibits axillary bud development in response to HT, providing new insights into how environmental cues shape plant architecture.

Hyperhidrosis is characterized by excessive sweating, typically in the palmar and axillary regions. Individuals with severe cases of hyperhidrosis can be treated surgically via endoscopic thoracic sympathectomy to disrupt the neural connection between the spinal cord and the affected regions, thereby attenuating sweating in the hyperhidrotic regions. However, the effects of this procedure on skin blood flow and sweating responses to whole body heat stress in regions not targeted by the sympathectomy, such as the forearm, are unknown. We tested the hypothesis that surgical sympathectomy attenuates the increase in forearm cutaneous vascular conductance and sweating during whole body heat stress. Before and 7 ± 1 wk following bilateral thoracic surgical sympathectomy, forearm skin blood flow (laser-Doppler imaging) and local sweat rate (capacitance hygrometry) were assessed during whole body passive heat stress sufficient to elevate core temperature by ∼1°C (P = 0.74 between trials) in 10 subjects (27 ± 3 yr; 7 females). The mean increase in forearm cutaneous vascular conductance was attenuated following sympathectomy (Δ3.67 ± 1.34 flux·mmHg[-1] vs. Δ1.62 ± 1.19 flux·mmHg[-1]; P < 0.01). Similarly, mean sweat rate was attenuated in the palmar (Δ0.68 ± 0.42 mg·min[-1]·cm[-2] vs. Δ0.20 ± 0.25 mg·min[-1]·cm[-2]; P = 0.015) and forearm (Δ0.62 ± 0.31 mg·min[-1]·cm[-] vs. Δ0.24 ± 0.26 mg·min[-1]·cm[-2]; P = 0.03) regions following sympathectomy. These data suggest that the increase in forearm cutaneous vascular conductance and sweat rate in response to whole body heat stress is attenuated by ∼50% after surgical sympathectomy. However, the implications of these responses on whole body thermoregulation remain unknown.NEW & NOTEWORTHY Thoracic surgical sympathectomy is often performed to attenuate sweating in the palmar and axillary regions in individuals with hyperhidrosis. However, the effect of this procedure on efferent thermoregulatory responses to heat stress is unknown. We show that the increase in forearm cutaneous vascular conductance and local sweat rate is attenuated during whole body passive heating following a surgical sympathectomy.

Rapid biodosimetry at the point of care is critical for efficient triage and clinical management during mass-casualty radiological events. Here, we introduce a power-free biodosimetry platform integrating one-step reverse transcription recombinase polymerase amplification (RT-RPA) with vertical flow immunoassay (VFI) for the multiplex detection of two radiation-responsive transcripts (CDKN1A and DDB2) and housekeeping gene (MRPS5) from fingerstick blood. One-step RT-RPA showed optimal efficiency at 36 °C for 20 min, comparable to two-step RT-RPA and standard PCR. This temperature could be provided by the human body, where the axilla delivered a stable heat source (36.2 °C) with minimal interindividual variability across a range of environmental conditions (from 4 to 42 °C), supporting amplification comparable to thermocycler-based reactions. Amplified products were detected using a capillary-driven VFI platform. The assay demonstrated strong specificity, uniform signal distribution, and reproducibility with intra- and interassay coefficient of variation below 10% and 15%, respectively, across all three transcripts. When applied to ex vivo X-ray irradiated blood samples (1 and 2 Gy), a dose-dependent increase in CDKN1A and DDB2 signals was observed. Receiver operating characteristic analysis demonstrated that discrimination between sham- and 1 Gy-irradiated was not significant, whereas the assay distinguished sham- from 2 Gy-irradiated with area under the curve values of 0.82 (95% CI = [0.66-0.98]; p = 0.0052) and 0.89 (95% CI = [0.76-1.00]; p = 0.0006) for CDKN1A and DDB2, yielding sensitivity/specificity of 84.62%/69.23% and 92.31%/84.62%, respectively. These findings supported the feasibility of the body-heat one-step RT-RPA VFI as a rapid, equipment-free, field-deployable triage tool for large-scale radiation biodosimetry.

Vegetatively propagated sugarcane can accumulate multiple viruses that compromise planting-material health. Here, we present a model-guided alternating high-temperature thermotherapy (AHTT) protocol to eliminate major viruses from diverse sugarcane cultivars. We describe preparation and disinfection of single-bud axillary-bud cuttings, planting, thermal preconditioning, and a 12-day AHTT regimen. We then detail post-thermotherapy recovery, health scoring, leaf sampling, total-RNA extraction, control-validated one-step RT-PCR, result interpretation, and the detection of additional sugarcane viruses. For complete details on the use and execution of this protocol, please refer to Huang et al.[1].