▪ Abstract Occupational low back pain (LBP) is an immense burden for both industry and medicine. Ergonomic and personal risk factors result in LBP, but psychosocial factors can influence LBP disability. Epidemiologic studies clearly indicate the role of mechanical loads on the etiology of occupational LBP. Occupational exposures such as lifting, particularly in awkward postures; heavy lifting; or repetitive lifting are related to LBP. Fixed postures and prolonged seating are also risk factors. LBP is found in both sedentary occupations and in drivers as well as those involved in manual materials handling. Any prolonged posture will lead to static loading of the soft tissues and cause discomfort. Standing and sitting have specific advantages and disadvantages for mobility, exertion of force, energy consumption, circulatory demands, coordination, and motion control. The seated posture leads to inactivity causing an accumulation of metabolites, accelerating disk degeneration and leading to disk herniation. Driver's postures can also lead to musculoskeletal problems. Workers in a driving environment are often subjected to postural stress leading to back, neck, and upper extremity pain. This exacerbates the problems due to the vibration. Prevention is by far the treatment of choice. Improved muscle function can be preventative. Poor coordination and motor control systems are as important as endurance and strength. Fixed postures should be avoided. Seats offering good lumbar support should be used in the office. A suspension seat should be used in vehicles whenever possible. Heavy and awkward lifting should be avoided and lifting aids should be made available. Workers should report LBP as early as possible and seek medical advice if they think occupational exposure is harming them. The combined effects of the medical community, labor, and management are required to cause some impact on this problem.

Environmental pollution, such as air, water, and soil pollution, has become the most serious issue. Soil pollution is a major concern as it generally affects the lands and makes them non-fertile. The main cause of soil pollution is agro-waste. It may be possible to mitigate the agro-waste pollution by re-utilizing this agro-waste, namely natural fibres (NFs), by blending into polymer-based material to reinforce the polymer composite. However, there are pros and cons to this approach. Consequently, the polymer composite materials fabricated using NFs are inferior to those polymer composites that are reinforced by, e.g., carbon or glass fibres from the mechanical properties’ perspectives. The limitations of utilizing natural fibres in polymer matrix are their high moisture absorption, resulting in high swelling rate and degradation, inferior resistance to fire and chemical, and inferior mechanical properties. In particular, the NF polymer composites exhibit inferior interfacial adhesion between the fibre and the matrix, which, if improved, ultimately overcome all the listed limitations and improve the mechanical properties of the developed composites. To improve the interfacial adhesion leading to the enhancement of the mechanical properties, optimum chemical treatment such as Alkalization/Mercerization of the fibres have been explored. This article discusses the Mercerization/Alkali surface treatment method for NFs and its effects on the fibres regarding the Mercerization/Alkali surface treatment method for NFs and its effect on the fibres regarding their utilization in the polymer composites, the morphological features, and mechanical properties of composites.

Poly (lactic acid) (PLA)/natural halloysite nanotubes (HNTs) films were prepared by solution casting method to investigate their properties for packaging applications. Tensile test results revealed that the maximum tensile elastic modulus (1.40 ± 0.05 GPa) and tensile strength (52.75 ± 1.80 MPa) were achieved at 5 w/w % of HNTs (in a range of 0–10 w/w % HNT concentrations). A nanoindentation test was performed to confirm the reinforcing effect of HNTs. Analysis of electron micrographs of the fracture surfaces suggested that the reinforcing mechanism was subjected to the interfacial interaction between HNTs and PLA. Infrared spectra revealed that the end hydroxyl groups of PLA chemically interacted with HNTs’ outer surface siloxane groups via hydrogen bonding. In addition, the contact angle test and thermogravimetric analysis were used to investigate the surface wettability and thermal stability of the PLA/HNT films, respectively.

Summary: The age‐related loss of skeletal muscle mass and function (sarcopenia) is a consistent hallmark of ageing. Apoptosis plays an important role in muscle atrophy, and the intent of this study was to specify whether apoptosis is restricted to myofibre nuclei (myonuclei) or occurs in satellite cells or stromal cells of extracellular matrix (ECM). Sarcopenia in mouse gastrocnemius muscle was characterized by myofibre atrophy, oxidative type grouping, delocalization of myonuclei and ECM fibrosis. Terminal deoxynucleotidyl transferase‐mediated dUTP nick end‐labelling (TUNEL) indicated a sharp rise in apoptosis during ageing. TUNEL coupled with immunostaining for dystrophin, paired box protein‐7 (Pax7) or laminin‐2α, respectively, was used to identify apoptosis in myonuclei, satellite cells and stromal cells. In adult muscle, apoptosis was not detected in myofibres, but was restricted to stromal cells. Moreover, the age‐related rise in apoptotic nuclei was essentially due to stromal cells. Myofibre‐associated apoptosis nevertheless occurred in old muscle, but represented < 20% of the total muscle apoptosis. Specifically, apoptosis in old muscle affected a small proportion (0.8%) of the myonuclei, but a large part (46%) of the Pax7⁺ satellite cells. TUNEL coupled with CD31 immunostaining further attributed stromal apoptosis to capillary endothelial cells. Age‐dependent rise in apoptotic capillary endothelial cells was concomitant with altered levels of key angiogenic regulators, perlecan and a perlecan domain V (endorepellin) proteolytic product. Collectively, our results indicate that sarcopenia is associated with apoptosis of satellite cells and impairment of capillary functions, which is likely to contribute to the decline in muscle mass and functionality during ageing.

Connective tissues are biological composites comprising of collagen fibrils embedded in (and reinforcing) the hydrated proteoglycan-rich (PG) gel within the extracellular matrices (ECMs). Age-related changes to the mechanical properties of tissues are often associated with changes to the structure of the ECM, namely, fibril diameter. However, quantitative attempts to correlate fibril diameter to mechanical properties have yielded inconclusive evidence. Here, we described a novel approach that was based on the rule of mixtures for fiber composites to evaluate the dependence of age-related changes in tendon tensile strength $(σ)$ and stiffness $(E)$ on the collagen fibril cross-sectional area fraction $(ρ)$, which is related to the fibril volume fraction. Tail tendons from C57BL6 mice from age groups $1.6–35.3months$ old were stretched to failure to determine $σ$ and $E$. Parallel measurements of $ρ$ as a function of age were made using transmission electron microscopy. Mathematical models (rule of mixtures) of fibrils reinforcing a PG gel in tendons were used to investigate the influence of $ρ$ on ageing changes in $σ$ and $E$. The magnitudes of $σ$, $E$, and $ρ$ increased rapidly from $1.6monthsto4.0months$ ($P$-values $<0.05$) before reaching a constant (age independent) from $4.0monthsto29.0months$ ($P$-values $>0.05$); this trend continued for $E$ and $ρ$ ($P$-values $>0.05$) from $29.0monthsto35.3months$, but not for $σ$, which decreased gradually ($P$-values $<0.05$). Linear regression analysis revealed that age-related changes in $σ$ and $E$ correlated positively to $ρ$ ($P$-values $<0.05$). Collagen fibril cross-sectional area fraction $ρ$ is a significant predictor of ageing changes in $σ$ and $E$ in the tail tendons of C57BL6 mice.